AbstractThe glucagon-like peptide-1 (GLP-1) receptor, known as GLP-1R, is a vital component of the G protein-coupled receptor (GPCR) family and is found primarily on the surfaces of various cell types within the human body. This receptor specifically interacts with GLP-1, a key hormone that plays an integral role in regulating blood glucose levels, lipid metabolism, and several other crucial biological functions.

摘要胰高血糖素样肽-1（GLP-1）受体，称为GLP-1R，是G蛋白偶联受体（GPCR）家族的重要组成部分，主要存在于人体内各种细胞类型的表面。该受体与GLP-1特异性相互作用，GLP-1是一种关键激素，在调节血糖水平，脂质代谢和其他几种关键生物学功能中起着不可或缺的作用。

In recent years, GLP-1 medications have become a focal point in the medical community due to their innovative treatment mechanisms, significant therapeutic efficacy, and broad development prospects. This article thoroughly traces the developmental milestones of GLP-1 drugs, from their initial discovery to their clinical application, detailing the evolution of diverse GLP-1 medications along with their distinct pharmacological properties.

。本文彻底追踪了GLP-1药物的发展里程碑，从最初的发现到临床应用，详细介绍了各种GLP-1药物的演变及其独特的药理学特性。

Additionally, this paper explores the potential applications of GLP-1 receptor agonists (GLP-1RAs) in fields such as neuroprotection, anti-infection measures, the reduction of various types of inflammation, and the enhancement of cardiovascular function. It provides an in-depth assessment of the effectiveness of GLP-1RAs across multiple body systems-including the nervous, cardiovascular, musculoskeletal, and digestive systems.

此外，本文探讨了GLP-1受体激动剂（GLP-1RAs）在神经保护，抗感染措施，减少各种炎症和增强心血管功能等领域的潜在应用。它深入评估了GLP-1RAs在多个身体系统（包括神经系统，心血管系统，肌肉骨骼系统和消化系统）中的有效性。

This includes integrating the latest clinical trial data and delving into potential signaling pathways and pharmacological mechanisms. The primary goal of this article is to emphasize the extensive benefits of using GLP-1RAs in treating a broad spectrum of diseases, such as obesity, cardiovascular diseases, non-alcoholic fatty liver disease (NAFLD), neurodegenerative diseases, musculoskeletal inflammation, and various forms of cancer.

这包括整合最新的临床试验数据，并深入研究潜在的信号通路和药理机制。本文的主要目的是强调使用GLP-1RAs治疗广泛疾病的广泛益处，例如肥胖，心血管疾病，非酒精性脂肪肝病（NAFLD），神经退行性疾病，肌肉骨骼炎症和各种形式的癌症。

The ongoing development of new indications for GLP-1 drugs offers promi.

GLP-1药物新适应症的不断开发提供了前景。

IntroductionIn recent years, GLP-1R and its agonists have garnered widespread attention in the medical community. GLP-1R, a core member of the GPCR family, is widely present on the surfaces of various cells in the human body.1,2 By specifically binding to the key hormone GLP-1, it regulates blood glucose levels and lipid metabolism.3,4 This receptor and its agonists hold significant therapeutic potential, reshaping the treatment approaches for multiple diseases, including diabetes, cardiovascular disorders, and neurodegenerative diseases.5,6,7 GLP-1 is a peptide produced by the cleavage of proglucagon, mainly synthesized in the intestinal mucosal L-cells, pancreatic islet α-cells, and neurons in the nucleus of the solitary tract.3,4 GLP-1RAs mimic the action of endogenous GLP-1, activating GLP-1R, thereby enhancing insulin secretion, inhibiting glucagon release, delaying gastric emptying, and reducing food intake through central appetite suppression.8,9,10 These mechanisms make GLP-1RAs powerful tools for controlling blood glucose and improving metabolic syndrome.

引言近年来，GLP-1R及其激动剂在医学界引起了广泛关注。。

Furthermore, their multifaceted mechanisms of action suggest potential applications beyond traditional metabolic disorders. From the discovery of the GLP-1 fragment GLP-1(7-37) to the development of more stable and long-acting GLP-1 analogs, these milestones represent significant breakthroughs in the medical field.11,12 For instance, the success of exenatide has not only spurred the development of potent GLP-1 analogs such as liraglutide and semaglutide but also unveiled the vast potential of GLP-1RAs in treating various systemic diseases.

此外，它们的多方面作用机制表明其在传统代谢紊乱之外的潜在应用。从GLP-1片段GLP-1（7-37）的发现到更稳定和长效的GLP-1类似物的开发，这些里程碑代表了医学领域的重大突破[11,12]。例如，艾塞那肽的成功不仅刺激了利拉鲁肽和semaglutide等强效GLP-1类似物的开发，而且揭示了GLP-1RAs在治疗各种全身性疾病方面的巨大潜力。

These developments underscore the importance of GLP-1RAs in modern therapeutics. The applications of GLP-1RAs extend far beyond diabetes management.5Here we summarized the c.

这些发展强调了GLP-1RAs在现代治疗中的重要性。GLP-1RAs的应用远远超出了糖尿病管理的范围.5在这里，我们总结了c。

Dual agonists

双重激动剂

Dual agonists target both the GLP-1R and another specific receptor.124,129 A common combination is GLP-1 with GIP or insulin-like growth factor.130 For example, a popular dual agonist, tirzepatide (brand name Mounjaro), activates both GLP-1 and GIPR.124 GLP-1, by activating its receptor, increases insulin secretion and reduces glucagon secretion, thereby lowering blood sugar levels.131,132,133 Additionally, GLP-1 helps to delay gastric emptying and suppress appetite, aiding in weight management.121,134 GIP, another insulin secretion agonist, helps release insulin, particularly after eating, enhancing the effects of GLP-1 and thereby improving the overall therapeutic efficacy of the drug.125,130 In 2022, tirzepatide was approved by the FDA for the treatment of T2DM in the United States.135,136 It is considered a significant breakthrough in diabetes treatment and is also being studied for the treatment of obesity due to its significant weight loss effects.135 Tirzepatide is developed by Eli Lilly and has proven to provide superior blood sugar control and significant weight loss, making it particularly valuable in the treatment of T2DM.136,137,138 Research and clinical trials have shown that tirzepatide not only improves blood sugar levels but also has a positive impact on cardiovascular risk factors.139,140,141 Although dual agonists show advantages in efficacy, their safety and tolerability continue to be a focus of ongoing monitoring.141 Common side effects include gastrointestinal reactions, such as nausea and vomiting, which are typically more common during the initial stages of treatment.141,142 The Phase III clinical trials of tirzepatide were conducted in 77 research centers across seven countries, including the United States, Brazil, and Japan.143 The trials recru.

双重激动剂靶向GLP-1R和另一种特异性受体。124129一种常见的组合是GLP-1与GIP或胰岛素样生长因子。130例如，一种流行的双重激动剂tirzepatide（商标名Mounjaro）激活GLP-1和GIPR.124 GLP-1通过激活其受体，增加胰岛素分泌并减少胰高血糖素分泌，从而降低血糖水平。131132133此外，GLP-1有助于延迟胃排空和抑制食欲，有助于体重管理。121134另一种胰岛素分泌激动剂GIP有助于释放胰岛素，特别是在进食后，增强GLP-1的作用，从而提高药物的整体治疗效果。125130 2022年，替罗西肽被FDA批准用于治疗美国的T2DM。135136它被认为是糖尿病治疗的一个重大突破，由于其显着的减肥作用，也正在研究用于治疗肥胖症。135替罗西肽由礼来公司开发，已被证明可提供优异的血糖控制和显着的体重减轻，使其在T2DM的治疗中特别有价值。136137138研究和临床试验表明，替罗西肽不仅可以改善血糖水平，还可以对心血管危险因素产生积极影响。139140141虽然双激动剂在疗效上显示出优势，但其安全性和耐受性仍然是持续监测的重点。141常见的副作用包括胃肠道反应，如恶心和呕吐，通常在治疗的初始阶段更为常见。141142在七个国家的77个研究中心进行了tirzepatide的III期临床试验，包括美国，巴西和日本.143审判重新开始。

Triple agonist

三重激动剂

Triple agonists go even further.148 These drugs act by simultaneously targeting three different agonists GLP-1R, the GIPR, and the GCGR.149,150,151 These receptors each have independent yet complementary roles in the treatment of diabetes and obesity.150,152,153 Activation of the GLP-1R can enhance insulin secretion, reduce glucagon secretion, delay gastric emptying,154 and suppress appetite.155,156 GIPR activation also promotes insulin release, especially after meals, helping to improve glucose utilization.157,158 Activation of the insulin or Insulin-like Growth Factor 1 (IGF-1) receptor can enhance insulin sensitivity, improve glucose absorption and utilization by cells, and potentially have positive effects on cardiovascular health and long-term energy balance.159 As of now, GLP-1-related triple agonists are primarily still in the development stage and have not been widely approved for use.159 These drugs are not yet widely available on the market but have shown some potential in clinical trials.160,161 For example, HM15211, a triple agonist developed by Hanmi Pharmaceutical in South Korea that activates GLP-1R, GIPR and GCGR has entered early clinical trials for the treatment of obesity and non-alcoholic steatohepatitis (NASH).162,163 Retatrutide (LY-3437943), a novel triple agonist developed by Eli Lilly that targets GLP-1R, GIPR and GCGR, has shown potential in preliminary clinical data for providing excellent blood sugar control and significant weight reduction.158,161,164,165 However, activating multiple receptors may lead to more complex side effects, and in some experiments, dual and triple agonists have indeed shown more severe side effects.165,166 Retatrutide has now entered Phase III clinical trials.161 The results of the Phase II clinical trials of retatru.

三重激动剂走得更远。148这些药物通过同时靶向三种不同的激动剂GLP-1R，GIPR和GCGR起作用。149150151这些受体在治疗糖尿病和肥胖症方面都具有独立但互补的作用。150152153激活GLP-1R可以增强胰岛素分泌，减少胰高血糖素分泌，延迟胃排空，154和抑制食欲。155156 GIPR激活也促进胰岛素释放，特别是饭后，有助于提高葡萄糖利用率。157158激活胰岛素或胰岛素样生长因子1（IGF-1）受体可以增强胰岛素敏感性，改善细胞对葡萄糖的吸收和利用，并可能对心血管健康和长期产生积极影响-term能量平衡.159截至目前，与GLP-1相关的三重激动剂主要仍处于开发阶段，尚未被广泛批准使用。159这些药物尚未在市场上广泛销售，但已在临床试验中显示出一定的潜力。160161例如，HM15211是韩国汉米制药开发的一种三重激动剂，可激活GLP-1R，GIPR和GCGR，已进入治疗肥胖和非酒精性脂肪性肝炎（NASH）的早期临床试验。162163瑞曲肽（LY-3437943）是礼来公司开发的一种新型三重激动剂，靶向GLP-1R，GIPR和GCGR，在初步临床数据中显示出提供优异的潜力血糖控制和显着减肥.158161164165然而，激活多种受体可能会导致更复杂的副作用，在一些实验中，双重和三重激动剂确实显示出更严重的副作用.165166瑞他曲肽现已进入III期临床试验.161瑞他曲II期临床试验的结果。

In summary, dual and triple agonists related to GLP-1 represent significant advances in the field of diabetes treatment,167,168 demonstrating the future trend of enhancing therapeutic effects by targeting multiple biomarkers.136,169,170 With the accumulation of more clinical data and the development of new drugs, these treatment options are expected to provide more effective and comprehensive treatment choices for diabetes patients.161,167.

总之，与GLP-1相关的双重和三重激动剂代表了糖尿病治疗领域的重大进展，167168证明了通过靶向多种生物标志物来增强治疗效果的未来趋势.136169170随着更多临床数据的积累和新药的开发，这些治疗方案有望为糖尿病患者提供更有效和全面的治疗选择.161167。

Small molecule GLP-1RAsCurrently, most GLP-1RAs are based on proteins or peptides, meaning they are large molecules typically administered via injection.37 Small molecule GLP-1RAs are chemically synthesized, and compared to protein-based drugs, they generally have smaller molecular sizes.171 The development of small molecule GLP-1RAs aims to overcome some of the limitations of traditional protein or peptide-based GLP-1RAs, such as the need for injection.

小分子GLP-1目前，大多数GLP-1RAs基于蛋白质或肽，这意味着它们是通常通过注射给药的大分子.37小分子GLP-1RAs是化学合成的，与基于蛋白质的药物相比，它们通常具有较小的分子大小.171小分子GLP-1RAs的开发旨在克服传统蛋白质或基于肽的GLP-1RAs的一些局限性，例如需要注射。

Small molecule drugs may offer the possibility of oral administration, which is more convenient and acceptable for patients.171 Additionally, small molecule drugs may have better tissue permeability, longer half-lives in the body, and lower production costs. As of now, research on small molecule GLP-1RAs is still mainly in the laboratory and early clinical trial stages.172 The challenges in developing these drugs include ensuring that they can effectively mimic the biological activity of large molecule GLP-1RAs while maintaining efficacy and selectivity.

小分子药物可能提供口服给药的可能性，这对患者来说更方便和可接受.171此外，小分子药物可能具有更好的组织渗透性，更长的半衰期和更低的生产成本。到目前为止，对小分子GLP-1RAs的研究仍主要处于实验室和早期临床试验阶段.172开发这些药物的挑战包括确保它们能够有效模拟大分子GLP-1RAs的生物活性，同时保持功效和选择性。

This review article will introduce some of the small molecule drugs that are currently receiving significant attention:.

这篇综述文章将介绍一些目前备受关注的小分子药物：。

Orforglipron

奥尔福格里普龙

Orforglipron is an oral small molecule GLP-1RA developed jointly by Eli Lilly and Chia Tai Tianqing Pharmaceutical Group.173 Its research findings were recently presented orally at the 83rd Scientific Sessions of the American Diabetes Association and published in the New England Journal of Medicine.

Orforglipron是礼来公司和正大天青制药集团联合开发的一种口服小分子GLP-1RA。173其研究结果最近在美国糖尿病协会第83届科学会议上口头发表，并发表在《新英格兰医学杂志》上。

In a 26-week study, orforglipron demonstrated a significant dose-dependent effect on weight loss, with weight reduction ranging from 8.6% to 12.6% across various dosages, compared to only 2.0% in the placebo group. By week 36, this weight loss effect was even more pronounced, increasing from 9.4% to 14.7%, while the placebo group saw a reduction of only 2.3%.

在一项为期26周的研究中，orforglipron对体重减轻具有显着的剂量依赖性作用，不同剂量的体重减轻范围为8.6%至12.6%，而安慰剂组仅为2.0%。。

Additionally, in another Phase II study targeting patients with T2DM, orforglipron also showed significant effects in reducing A1C and weight, achieving the study’s primary and secondary endpoints. In this study, participants taking orforglipron experienced an average A1C reduction of 2.1% and an average weight loss of 10.1 kilograms at 26 weeks, which was significantly greater than those in the placebo and dulaglutide groups.

此外，在另一项针对T2DM患者的II期研究中，orforglipron在降低A1C和体重方面也显示出显着效果，达到了研究的主要和次要终点。在这项研究中，服用orforglipron的参与者在26周时平均A1C降低了2.1%，平均体重减轻了10.1公斤，这明显高于安慰剂组和杜拉鲁肽组。

Between 65% and 96% of participants taking orforglipron achieved an A1C level below 7.0% at 26 weeks.174 Currently, Eli Lilly has initiated a Phase III development program to further investigate the efficacy and safety of orforglipron in treating obesity, overweight, and T2DM..

服用orforglipron的参与者中有65%至96%在26周时A1C水平低于7.0%.174目前，礼来公司已经启动了一项III期开发计划，以进一步研究orforglipron治疗肥胖，超重和T2DM的疗效和安全性。。

Danuglipron

Danuglipron

Danuglipron is an oral GLP-1RA developed by Pfizer. In May 2023, Pfizer released the results of a Phase 2b clinical trial of the drug. The study involved 411 adult patients with T2DM and was designed as a randomized, double-blind, placebo-controlled trial where patients received varying doses of danuglipron or a placebo.

Danuglipron是辉瑞公司开发的口服GLP-1RA。2023年5月，辉瑞公司公布了该药物2b期临床试验的结果。这项研究涉及411名成年T2DM患者，设计为一项随机，双盲，安慰剂对照试验，患者接受不同剂量的达努格列隆或安慰剂。

The results showed that during the 16-week treatment period, patients who received the highest dosage (120 mg twice daily) of danuglipron experienced an average reduction in HbA1c of 1.16 percentage points and a weight loss of 4.17 kilograms. All dosages of danuglipron significantly reduced patients’ HbA1c and fasting blood glucose levels, with more pronounced weight loss effects observed in the 80 mg and 120 mg doses compared to the placebo group.

结果显示，在16周的治疗期间，接受最高剂量（120 mg，每日两次）达努格列隆的患者HbA1c平均降低1.16个百分点，体重减轻4.17公斤。与安慰剂组相比，所有剂量的达努格列隆均显着降低患者的HbA1c和空腹血糖水平，在80mg和120mg剂量下观察到更明显的减肥效果。

Common adverse reactions included nausea, diarrhea, and vomiting.172.

常见的不良反应包括恶心，腹泻和呕吐。

GSBR-1290

GSBR-1290

GSBR-1290 is an oral small molecule GLP-1RA developed by Structure Therapeutics, aimed at treating T2DM and obesity. On December 18, 2023, Structure Therapeutics published the latest clinical data for GSBR-1290 on its official website.175 Currently, GSBR-1290 is undergoing a 12-week Phase 2a randomized, double-blind, placebo-controlled clinical trial to assess its effectiveness in treating patients with T2DM and obesity.

GSBR-1290是由Structure Therapeutics开发的口服小分子GLP-1RA，旨在治疗T2DM和肥胖症。2023年12月18日，Structure Therapeutics在其官方网站上发布了GSBR-1290的最新临床数据。目前，GSBR-1290正在进行为期12周的2a期随机，双盲，安慰剂对照临床试验，以评估其治疗T2DM和肥胖患者的有效性。

To date, the trial has enrolled 94 participants, with 54 in the T2DM group and 40 in the obesity group. Regarding safety, the majority of reported adverse events were mild to moderate, ranging from 88% to 96%, depending on the specific study group. Among the 60 participants treated with GSBR-1290, only one (2.8%, from the T2DM group) discontinued the study due to drug-related adverse events (AEs).

迄今为止，该试验已招募了94名参与者，其中T2DM组54名，肥胖组40名。关于安全性，根据具体的研究组，大多数报告的不良事件是轻度至中度的，范围从88%到96%。在接受GSBR-1290治疗的60名参与者中，只有一名（2.8%，来自T2DM组）由于药物相关不良事件（AE）停止了研究。

As for clinical outcomes, in the T2DM group, there was a significant reduction in HbA1c (decreased by 1.01% to 1.02%, placebo-adjusted) and a clinically meaningful decrease in body weight of 3.26% to 3.51% after 12 weeks of treatment. In the obesity group, there was a significant and clinically meaningful reduction in body weight of 4.74% at week 8, with weight continuously decreasing during the 8-week treatment period.175.

至于临床结果，在T2DM组中，治疗12周后HbA1c显着降低（降低1.01%至1.02%，安慰剂调整），临床上有意义的体重下降3.26%至3.51%。在肥胖组中，第8周体重显着降低4.74%，在8周治疗期间体重持续下降。

Classical pathophysiological mechanisms of GLP-1GLP-1 signaling pathwayGLP-1 initiates signaling by binding to its receptor, GLP-1R, which is a G-protein-coupled receptor.176,177 When GLP-1 binds to GLP-1R, it triggers the activation of G-proteins, leading to an increase in the intracellular second messenger cAMP.34,39,177 The rise in cAMP activates protein kinase A (PKA), which then promotes the synthesis and secretion of insulin and inhibits the release of glucagon.178,179 Additionally, cAMP can activate Rap1 through EPAC (Exchange Protein directly Activated by cAMP),180,181,182 which is involved in regulating insulin secretion.180,181,183 GLP-1 also activates the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) pathway, which is crucial for maintaining the survival and function of pancreatic β-cells.184,185,186,187Interactions with other pathwaysGLP-1 not only promotes the release of insulin but also enhances the response of pancreatic β-cells to insulin through the PI3K/Akt pathway, thereby improving insulin signal transduction and increasing the sensitivity of peripheral tissues to insulin.1,188 GLP-1 reduces hepatic glucose production, partly by inhibiting the expression and activity of key gluconeogenic enzymes.189,190,191 Activation of GLP-1R leads to the production of cAMP (cyclic Adenosine Monophosphate), which is achieved by activating Adenylyl Cyclase (AC).191,192 Following the activation of GLP-1R, the βγ subunits of GPCRs can directly activate Class I PI3Ks.1 These PI3Ks typically include the PI3Kα and PI3Kβ isoforms, which are composed of regulatory subunits containing SH2 domains and catalytic subunits.193 These subunits can directly interact with the activated GPCR or do so via intermediary proteins such as insulin receptor substrate.194,195 The .

GLP-1GLP-1信号通路的经典病理生理机制GLP-1通过与其受体GLP-1R结合来启动信号传导，GLP-1R是一种G蛋白偶联受体.176177当GLP-1与GLP-1R结合时，它触发G蛋白的激活，导致细胞内第二信使cAMP的增加[34,39177]。cAMP的升高激活蛋白激酶a（PKA），然后促进胰岛素的合成和分泌，抑制胰高血糖素的释放[178179]。此外，cAMP可以通过EPAC（由cAMP直接激活的交换蛋白）激活Rap1，180181182参与调节胰岛素分泌。180181183 GLP-1还激活磷酸肌醇3-激酶（PI3K）/蛋白激酶B（Akt）途径，这对于维持胰腺β-cells的存活和功能至关重要。184185186187与其他途径的相互作用GLP-1不仅促进胰岛素的释放，而且通过PI3K/Akt途径增强胰腺β细胞对胰岛素的反应，从而改善胰岛素信号转导并提高外周组织对胰岛素的敏感性。1188 GLP-1减少了肝脏葡萄糖的产生，部分是通过抑制关键糖异生酶的表达和活性。189190191 GLP-1R的激活导致产生cAMP（环磷酸腺苷），这是通过激活腺苷酸环化酶（AC）实现的。191192在GLP-1R激活后，GPCR的βγ亚基可以直接激活I类PI3K。这些PI3K通常包括PI3Kα和PI3Kβ亚型，它们由含有SH2结构域和催化亚基的调节亚基组成。193这些亚基可以直接与活化的GPCR相互作用，也可以通过胰岛素受体底物等中间蛋白相互作用。

GLP-1RAs in OA

骨关节炎中的GLP-1RA

GLP-1R expression was detected via immunohistochemistry in articular chondrocytes from both normal and osteoarthritic individuals.273 The primary outcome of GLP-1R expression involves suppressing the release of cytokines into the synovial fluid, leading to a reduction in inflammation.274,275 This, in turn, diminishes additional downstream effects, including oxidative stress, the secretion of pro-degradative substances, modifications to cell phenotype (hypertrophy, M1/M2 macrophage phenotype, fibrosis), and damage or deterioration of joint cells (apoptosis, senescence).15,276.

GLP-1R表达通过免疫组织化学在正常人和骨关节炎患者的关节软骨细胞中检测到.273 GLP-1R表达的主要结果涉及抑制细胞因子释放到滑液中，导致炎症减少.274275这反过来又减少了额外的下游效应，包括氧化应激，促降解物质的分泌，细胞表型的改变（肥大，M1/M2巨噬细胞表型，纤维化）以及关节细胞的损伤或恶化（细胞凋亡，衰老）.15276。

The activation of GLP-1R is linked to decreased NF-κB pathway activity Treatment with GLP-1RAs can effectively mitigate chondrocyte apoptosis caused by endoplasmic reticulum stress and alleviate the associated inflammatory response.277,278,279,280 This effect is accomplished through the inhibition of JNK, NF-κB, and other relevant signaling pathways.273 Moreover, GLP-1RAs could decelerate the progression of OA and mitigate pathological damage in a rat OA model.273 In addition, in a rat model of inflammatory OA induced by monoiodoacetic acid (MIA), researchers have shown that the activation of GLP-1R triggers the PKA/CREB signaling pathway, leading to a reduction in cartilage inflammation.281.

GLP-1R的激活与NF-κB通路活性降低有关。用GLP-1RAs治疗可以有效减轻内质网应激引起的软骨细胞凋亡，减轻相关的炎症反应。277278279280这种作用是通过抑制JNK，NF-κB和其他相关信号通路来实现的。此外，GLP-1RAs可以减缓OA的进展，减轻大鼠OA模型的病理损伤。273此外，在由单碘乙酸（MIA）诱导的炎性OA大鼠模型中，研究人员表明，GLP-1R的激活触发PKA/CREB信号通路，导致减少软骨炎症。

Inflammation in OA is closely related to the activation of macrophages.282,283 These cells accumulate in the synovial membrane and subchondral bone, releasing pro-inflammatory cytokines such as TNF-α, IL-1β, and IL-6, which promote the degradation of joint cartilage and the inflammatory response.284,285,286 Macrophages express GLP-1Rs, which are involved in regulating their inflammatory responses.

OA中的炎症与巨噬细胞的活化密切相关[282283]。这些细胞在滑膜和软骨下骨中积累，释放促炎细胞因子，如TNF-α，IL-1β和IL-6，促进关节软骨的降解和炎症反应[284285286]。巨噬细胞表达GLP-1Rs，参与调节其炎症反应。

Binding of GLP-1 or GLP-1RAs to these receptors can activate the cAMP/PKA signaling pathway, affecting key transcription factors like NF-κB.287,288.

GLP-1或GLP-1RAs与这些受体的结合可以激活cAMP/PKA信号通路，影响关键的转录因子，如NF-κB.287288。

This binding initiates typical GPCR signaling, leading to G protein activation and increased intracellular cAMP.289 The rise in cAMP activates PKA, a versatile protein kinase that phosphorylates various target proteins.290,291,292 In macrophages, PKA regulates gene expression by phosphorylating transcription factors like CREB.293 CREB activation can promote the expression of anti-inflammatory genes while inhibiting inflammatory genes.294,295 In inflammation regulation, NF-κB is a key transcription factor.296,297,298 Typically, NF-κB binds to its inhibitor IκB in the cytoplasm.297,299 When IκB is phosphorylated and degraded, NF-κB can move to the nucleus, activating multiple inflammation-related genes.300,301 This not only affects the intracellular signaling of macrophages but also their response to the external environment, including their effects on chondrocytes and other synovial cells.302,303,304,305.

这种结合启动了典型的GPCR信号传导，导致G蛋白活化和细胞内cAMP增加。289 cAMP的升高激活了PKA，PKA是一种多功能蛋白激酶，可磷酸化各种靶蛋白。290291292在巨噬细胞中，PKA通过磷酸化CREB等转录因子来调节基因表达。293 CREB激活可促进抗炎基因的表达，同时抑制炎症基因。294295在炎症调节中，NF-κB是关键的转录因子。296297298通常，NF-κB与细胞质中的抑制剂IκB结合。297299当IκB被磷酸化和降解时，NF-κB可以转移至细胞核，激活多种炎症相关基因.300301这不仅影响巨噬细胞的细胞内信号传导，还影响它们对外部环境的反应，包括它们对软骨细胞和其他滑膜细胞的影响.302303304305。

GLP-1R signaling, through PKA, inhibits this process, possibly by promoting IκB stability or inhibiting its phosphorylation, thus reducing NF-κB activation and nuclear translocation.8,281 Through these mechanisms, GLP-1R signaling influences the production of inflammatory factors in macrophages.306 For example, the reduction in TNF-α, IL-1β, and IL-6 helps regulate local and systemic inflammatory responses.307,308 Additionally, GLP-1R signaling may affect other macrophage functions, such as phagocytosis, migration, and cell survival.281.

GLP-1R信号通过PKA抑制这一过程，可能是通过促进IκB的稳定性或抑制其磷酸化，从而减少NF-κB的活化和核易位.8281通过这些机制，GLP-1R信号传导影响巨噬细胞中炎症因子的产生.306例如，TNF-α，IL-1β和IL-6的减少有助于调节局部和全身炎症反应.307308此外，GLP-1R信号传导可能影响其他巨噬细胞功能，如吞噬作用，迁移和细胞存活。

By reducing macrophage-mediated inflammatory responses, GLP-1RAs have the potential to alleviate symptoms of OA, including pain and joint stiffness.281,309 Moreover, reducing inflammation may slow down the degradation of joint cartilage, providing long-term joint protection.310,311 GLP-1RAs also enhance autophagy, a process of cellular clearance of damaged and outdated components.13,312 Regulation of autophagy may help remove harmful proteins and other cellular debris accumulated under inflammatory conditions, which is potentially important for maintaining the health of joint tissues.313,314.

通过减少巨噬细胞介导的炎症反应，GLP-1RAs有可能缓解OA的症状，包括疼痛和关节僵硬.281309此外，减少炎症可能会减缓关节软骨的降解，提供长期的关节保护.310311 GLP-1RAs也增强自噬，这是一种细胞清除受损和过时成分的过程.13312自噬的调节可能有助于去除炎症条件下积累的有害蛋白质和其他细胞碎片，这对于维持关节组织的健康可能很重要.313314。

In one study, OA was induced in rats by injecting MIA into the knee joint, mimicking the pathological changes of human OA.315 Subsequently, rats were treated with liraglutide through subcutaneous injection to observe its therapeutic effect on OA.315 The expression levels of GLP-1R, PKA/CREB signaling pathway components, and inflammation-related proteins (such as TNF-α, IL-1β, and IL-6) in the rat knee cartilage tissue were measured using Western blot and immunoprecipitation techniques.315 The results showed that, in the OA rat model, liraglutide could activate the PKA/CREB signaling pathway and inhibit the inflammatory response through this pathway, thereby alleviating OA symptoms.316 These findings provide scientific evidence for developing new OA treatment strategies, confirming the potential of GLP-1 agonists in treating OA.315,316,317.

在一项研究中，通过向膝关节注射MIA诱导大鼠OA，模拟人类OA的病理变化。随后，通过皮下注射利拉鲁肽治疗大鼠，观察其对OA的治疗效果。315使用蛋白质印迹和免疫沉淀技术测量大鼠膝关节软骨组织中GLP-1R，PKA/CREB信号通路成分和炎症相关蛋白（如TNF-α，IL-1β和IL-6）的表达水平。结果表明，在OA大鼠模型中，利拉鲁肽可以激活PKA/CREB信号通路并通过该通路抑制炎症反应，从而缓解炎症反应OA症状.316这些发现为开发新的OA治疗策略提供了科学证据，证实了GLP-1激动剂治疗OA的潜力.315316317。

GLP-1R is expressed in human monocyte-derived macrophages and the mouse macrophage cell line RAW264.7.279,318 c-Jun N-terminal kinase (JNK) is a mitogen-activated protein kinase (MAPK) involved in regulating cellular stress responses and inflammation.318 Signal Transducer and Activator of Transcription 3 (STAT3) is a transcription factor involved in cell growth, differentiation, and inflammatory responses.319,320,321 Researchers found that activation of GLP-1R could play a key role in regulating macrophage polarization by adjusting the phosphorylation levels of JNK and STAT3.318,322 Macrophages have two polarization states, M1 typically has pro-inflammatory properties, while M2 has anti-inflammatory properties.323,324,325 Specifically, activation of GLP-1R leads to an increase in cAMP levels, which in turn activates PKA, a widely regulating enzyme of cellular functions, capable of phosphorylating a variety of target proteins, thereby initiating the PKA/CREB signaling pathway.326,327 This not only prevents the phosphorylation of JNK but also promotes the phosphorylation of STAT3, aiding the shift of macrophages to an anti-inflammatory M2 phenotype.327 In the inflammatory environment, the M1 to M2 shift promoted by GLP-1 is crucial for reducing the expression of inflammatory factors such as IL-6, TNF-α, and iNOS.8,15,328.

GLP-1R在人单核细胞衍生的巨噬细胞中表达，小鼠巨噬细胞系RAW264.7.279318 c-Jun N末端激酶（JNK）是一种丝裂原活化蛋白激酶（MAPK），参与调节细胞应激反应和炎症.318信号转导和转录激活因子3（STAT3）是一种参与细胞生长，分化和炎症反应的转录因子.319320321研究人员发现，GLP-1R的激活可能通过调节JNK和STAT3的磷酸化水平在调节巨噬细胞极化中起关键作用.318322巨噬细胞具有两种极化状态，M1通常具有促炎特性，而M2具有323324325具体而言，GLP-1R的激活导致cAMP水平升高，进而激活PKA，PKA是一种广泛调节细胞功能的酶，能够磷酸化多种靶蛋白，从而启动PKA/CREB信号通路[326327]。这不仅可以防止JNK的磷酸化，还可以促进STAT3的磷酸化，有助于巨噬细胞向抗炎M2表型的转变[327]。在炎症环境中，由GLP-1促进的M1向M2的转变对于减少炎症因子如IL-6，TNF-α和iNOS的表达至关重要[8,15328]。

Chondrocytes are the only cell type in joint cartilage, responsible for synthesizing and maintaining the integrity of the cartilage matrix.329,330 In degenerative joint diseases like OA, the metabolic balance of chondrocytes is disrupted, leading to the overproduction of degrading enzymes and inflammatory mediators, including iNOS, MMP-13, and ADAMTS5 (a disintegrin and metalloproteinase with thrombospondin motifs 5), which participate in cartilage degradation and inflammatory processes.331 iNOS (inducible nitric oxide synthase) produces nitric oxide (NO) during inflammation, modulating signal transduction; MMP-13 (matrix metalloproteinase-13) is involved in cartilage degradation;331 ADAMTS5 is closely related to cartilage damage and inflammation.332,333,334 The NO produced by iNOS, as a free radical, can regulate intracellular signal transduction and modulate the inflammatory response.335,336 The expression of iNOS is primarily activated by the NF-κB pathway, which is activated and translocated to the nucleus upon inflammatory stimulation (such as bacterial endotoxins or pro-inflammatory cytokines), thus increasing the transcription and expression of iNOS.337,338,339 GLP-1 can exert its anti-inflammatory effects by activating its receptor, GLP-1R.339 When GLP-1 binds to GLP-1R, it activates the cAMP signaling pathway, leading to increased cAMP levels.1,340 The rise in cAMP further activates PKA, which can inhibit the NF-κB signaling pathway, reducing the production of inflammatory factors such as iNOS and other inflammation-related proteins.12,340,341 The expression of MMP-13 is regulated by IL-1β and TNF-α.

软骨细胞是关节软骨中唯一的细胞类型，负责合成和维持软骨基质的完整性.329330在OA等退行性关节疾病中，软骨细胞的代谢平衡被破坏，导致降解酶和炎症介质的过量产生，包括iNOS，MMP-13和ADAMTS5（一种具有血小板反应蛋白基序5的去整合素和金属蛋白酶），它们参与软骨降解和炎症过程.331 iNOS（诱导型一氧化氮合酶）在炎症过程中产生一氧化氮（NO），调节信号转导；MMP-13（基质金属蛋白酶-13）参与软骨降解；331 ADAMTS5与软骨损伤和炎症密切相关。332333334 iNOS产生的NO作为自由基可以调节细胞内信号转导并调节炎症反应。335336 iNOS的表达主要由NF-κB途径激活，NF-κB途径在炎症刺激（如细菌内毒素或促炎细胞因子）下被激活并转移到细胞核，从而增加iNOS的转录和表达。337338339 GLP-1可以通过激活其受体GLP-1R发挥其抗炎作用。339当GLP-1与GLP-1R结合时，它激活cAMP信号通路，导致增加cAMP水平.1340 cAMP的升高进一步激活PKA，PKA可以抑制NF-κB信号通路，减少炎症因子如iNOS和其他炎症相关蛋白的产生.12340341 MMP-13的表达受IL-1β和TNF-α的调节。

These factors promote the transcription of the MMP-13 gene by activating the MAPK and NF-κB signaling pathways.342,343,344 The GLP-1R signaling pathway may also af.

这些因子通过激活MAPK和NF-κB信号通路促进MMP-13基因的转录。342343344 GLP-1R信号通路也可能是af。

In another study, treatment of primary mouse chondrocytes with liraglutide reduced the mRNA expression levels of iNOS, MMP-13, and ADAMTS5, leading to a decrease in the secretion of inflammatory markers, including NO, prostaglandin E, and IL-6.348 Similarly, in human chondrocytes stimulated by TNF, GLP-1 analogs (such as liraglutide) showed an anti-catabolic effect, reducing the mRNA expression of MMP-3, MMP-13, and ADAMTS5.349,350 At the same time, the levels of two important components of the cartilage matrix, proteoglycans (a large molecule and a major component of the cartilage matrix) and type II collagen (the main structural protein of cartilage), increased.349,350 This change suggests that liraglutide not only inhibits inflammation and cartilage degradation but may also promote the synthesis and accumulation of cartilage matrix, thereby helping to protect and repair joint cartilage.273 Furthermore, a study using the anterior cruciate ligament transection (ACLT) rat model further confirmed that subcutaneous injection of liraglutide at 50 μg/kg/day, whether for 3 weeks or 6 weeks, could reduce OARSI scores, highlighting the potential of liraglutide in treating joint degeneration.273.

在另一项研究中，利拉鲁肽治疗原代小鼠软骨细胞可降低iNOS、MMP-13和ADAMTS5的mRNA表达水平，导致炎症标志物（包括NO、前列腺素E和IL-6.348）的分泌减少。同样，在TNF刺激的人软骨细胞中，GLP-1类似物（如利拉鲁肽）显示出抗分解代谢作用，降低了MMP-3、MMP-13和ADAMTS5.349350的mRNA表达。同时，软骨基质的两个重要成分蛋白多糖（软骨基质的大分子和主要成分）和II型胶原的水平（软骨的主要结构蛋白）增加。349350这一变化表明利拉鲁肽不仅可以抑制炎症和软骨降解，还可以促进软骨基质的合成和积累，从而有助于保护和修复关节软骨。273此外，一项使用前交叉韧带横断术（ACLT）的研究大鼠模型进一步证实，皮下注射利拉鲁肽50μg/kg/天，无论是3周还是6周，都可以降低OARSI评分，突出了利拉鲁肽治疗关节退变的潜力。

GLP-1RAs and RA

GLP-1RAs和RA

The role of GLP-1RA was also investigated in RA, which is characterized by chronic inflammation of the synovium and joint destruction. In fibroblast-like RA synoviocytes, the administration of lixisenatide resulted in a reduction in the inflammatory response.347 This was achieved by decreasing the expression of proinflammatory cytokines such as tumor necrosis factor (TNF), interleukin-6 (IL-6), and interleukin-8 (IL-8).15,351,352 Moreover, lixisenatide has been shown to inhibit matrix metalloproteinase (MMP) activity and effectively block various cell signaling pathways, including the JNK, activator protein-1, and NF-κB pathways.353 These findings confirm that in the synovium, GLP-1R is expressed on two different cell types, macrophages and fibroblast-like synoviocytes, which are specialized cells distributed within the synovial intima and subintima, and these cell types play important roles in hyaluronic acid synthesis, metabolite processing, and clearance of matrix degradation fragments.354.

还研究了GLP-1RA在RA中的作用，其特征在于滑膜的慢性炎症和关节破坏。在成纤维细胞样RA滑膜细胞中，利西那肽的给药导致炎症反应的减少。347这是通过降低促炎细胞因子如肿瘤坏死因子（TNF），白细胞介素-6（IL-6）和白细胞介素-8（IL-8）的表达来实现的。15351352此外，利西那肽已被证明可抑制基质金属蛋白酶（MMP）活性，并有效阻断各种细胞信号通路，包括JNK，激活蛋白-1和NF-κB通路。353这些发现证实，在滑膜中，GLP-1R在两种不同的细胞类型上表达，巨噬细胞和成纤维细胞样滑膜细胞是特化细胞分布在滑膜内膜和内膜下，这些细胞类型在透明质酸合成，代谢物加工和基质降解片段清除中起重要作用。

GLP-1RAs and musculoskeletal health

GLP-1RAs与肌肉骨骼健康

GLP-1RAs and bone

GLP-1RAs和骨骼

The quality of bone depends on bone metabolism, and the main factors affecting bone metabolism include osteoclasts, osteoblasts, and calcitonin.355,356,357 According to most related studies, osteoclasts and osteoblasts are indispensable for bone remodeling, and bone resorption and bone formation are mediated by osteoclasts and osteoblasts, respectively.358 GLP-1R is present in bone marrow stem cells (BMSCs),15,359 osteoblasts,15 osteocytes,360 and osteoclasts,361 and GLP-1RAs have the potential to impact these cells..

骨的质量取决于骨代谢，影响骨代谢的主要因素包括破骨细胞，成骨细胞和降钙素.355356357根据大多数相关研究，破骨细胞和成骨细胞对于骨重塑是必不可少的，骨吸收和骨形成分别由破骨细胞和成骨细胞介导.358 GLP-1R存在于骨髓干细胞（BMSCs），15359个成骨细胞，15个骨细胞，360和破骨细胞中，361和GLP-1RAs有可能影响这些细胞。。

GLP-1RAs and osteoclasts The greater degree of bone degradation observed in mice lacking GLP-1R indicates that GLP-1R signaling suppresses osteoclast differentiation and bone resorption.362 In an experimental study in which osteoclast formation and bone resorption were induced in mice through lipopolysaccharide (LPS) administration, researchers discovered that simultaneous treatment with exendin-4 resulted in a significant decrease in the number of osteoclasts, the proportion of bone resorption pits, and the levels of the bone resorption marker CTX compared to injection with LPS alone.363 According to previous reports, exendin-4, a GLP-1RA, has the potential to inhibit LPS-induced osteoclast formation and bone resorption in vivo.363,364 This inhibition is believed to occur through the suppression of LPS-induced TNF-α production in macrophages.15 Studies have indicated that GLP-1R KO mice exhibit greater numbers of osteoclasts and greater bone resorption than wild-type controls.364 Additionally, µCT analysis revealed that, compared with their wild-type counterparts, hyperlipidemic rats treated with subcutaneous GLP-1 for 3 days exhibited increased bone mass in the femur and vertebrae.365.

GLP-1RAs和破骨细胞在缺乏GLP-1R的小鼠中观察到的更大程度的骨降解表明GLP-1R信号传导抑制破骨细胞分化和骨吸收。362在一项实验研究中，通过脂多糖（LPS）给药诱导小鼠破骨细胞形成和骨吸收，研究人员发现，与单独注射LPS相比，同时用exendin-4治疗导致破骨细胞数量，骨吸收坑比例和骨吸收标志物CTX水平显着降低。363根据以前的报道，exendin-4（一种GLP-1RA）有可能抑制LPS诱导的破骨细胞形成和体内骨吸收。363364这种抑制作用被认为是通过抑制LPS诱导的巨噬细胞中TNF-α的产生而发生的。研究表明，GLP-1R KO小鼠表现出比野生型对照更多的破骨细胞数量和更大的骨吸收，μCT分析显示，与野生型相比，皮下GLP-1治疗3天的高脂血症大鼠股骨和椎骨骨量增加。

Diabetic patients have a higher risk of fractures than does the general population.366 Mice with type 1 diabetes (T1D) exhibit a reduction in bone mineral density (BMD) and compromised microstructural integrity.367 The administration of liraglutide also impeded osteoclastic bone formation, thereby inhibiting bone resorption and exerting protective effects on bone health in T1D mice.367 Specifically, liraglutide, both alone and in combination with insulin, effectively suppressed the formation of osteoclasts.

糖尿病患者的骨折风险高于普通人群.366患有1型糖尿病（T1D）的小鼠表现出骨密度（BMD）降低和微结构完整性受损.367利拉鲁肽的给药也阻碍了破骨细胞骨形成，从而抑制骨吸收并对T1D小鼠的骨健康产生保护作用.367具体而言，利拉鲁肽单独或与胰岛素联合使用可有效抑制破骨细胞的形成。

This effect is achieved by reducing the expression of Trem2 and NFATc1 and downregulating the expression of CTSK and TRAP to inhibit bone resorption activity. These findings provide further evidence for the impact of GLP-1RAs on osteoclastic bone resorption.367 A study involving 12-week-old ovariectomized mice revealed that administering liraglutide for 4 weeks effectively prevented the loss of trabecular bone.

这种效果是通过降低Trem2和NFATc1的表达并下调CTSK和TRAP的表达来抑制骨吸收活性来实现的。这些发现为GLP-1RAs对破骨细胞骨吸收的影响提供了进一步的证据.367一项涉及12周龄卵巢切除小鼠的研究表明，服用利拉鲁肽4周可有效防止小梁骨的丢失。

The analysis of bone tissue morphology revealed that there were no alterations in the rate of bone formation or in the levels of calcitonin or sclerostin in these mice. These findings suggest that liraglutide specifically reduces bone resorption without influencing bone formation.368.

骨组织形态分析显示，这些小鼠的骨形成速率或降钙素或硬化蛋白水平没有变化。这些发现表明利拉鲁肽特异性地减少骨吸收而不影响骨形成。

Since GLP-1R is expressed in thyroid C cells and GLP-1 directly stimulates the secretion of calcitonin, which is a potent inhibitor of bone resorption in osteoclasts, GLP-1 may contribute to the nutrient-mediated reduction in bone resorption.369,370 Genetic disruption of GLP-1R signaling leads to cortical osteopenia and heightened bone fragility, primarily caused by increased bone resorption by osteoclasts.

由于GLP-1R在甲状腺C细胞中表达，GLP-1直接刺激降钙素的分泌，降钙素是破骨细胞骨吸收的有效抑制剂，GLP-1可能有助于营养物质介导的骨吸收减少.369370 GLP-1R信号传导的遗传破坏导致皮质骨质减少和骨脆性增加，主要是由破骨细胞骨吸收增加引起的。

This change was accompanied by a decrease in thyroid calcitonin expression. Furthermore, the administration of exogenous GLP-1 resulted in elevated calcitonin expression in the thyroids of normal (wild-type) mice.362 The administration of calcitonin successfully reduced the levels of urinary deoxypyridinoline in GLP-1R knockout mice.

这种变化伴随着甲状腺降钙素表达的降低。此外，外源性GLP-1的给药导致正常（野生型）小鼠甲状腺中降钙素表达升高[362]。降钙素的给药成功降低了GLP-1R基因敲除小鼠尿脱氧吡啶啉的水平。

Additionally, treatment with GLP-1RA and exendin-4 increased the expression of the calcitonin gene in the thyroids of normal (wild-type) mice. These findings provide evidence that the regulatory influence of endogenous GLP-1R signaling on bone resorption is likely mediated through pathways that involve calcitonin.362 Considering the expression of the GLP-1R in thyroid C cells and the ability of GLP-1 to stimulate calcitonin secretion through a cAMP-mediated mechanism in vitro, it is plausible that calcitonin plays a role in the alterations in bone metabolism observed in GLP-1R-treated animals.369,370 Later, quantitative real-time PCR analysis demonstrated that the administration of exendin-4, a GLP-1RA, resulted in significant upregulation of thyroid calcitonin mRNA levels in wild-type mice.362.

此外，用GLP-1RA和exendin-4处理可增加正常（野生型）小鼠甲状腺中降钙素基因的表达。这些发现提供的证据表明，内源性GLP-1R信号传导对骨吸收的调节作用可能是通过涉及降钙素的途径介导的。考虑到GLP-1R在甲状腺C细胞中的表达以及GLP-1通过cAMP介导的机制刺激降钙素分泌的能力，降钙素在GLP-1R处理的动物中观察到的骨代谢改变中起作用似乎是合理的。369370后来，定量实时PCR分析表明，施用exendin-4（一种GLP-1RA）导致野生型小鼠甲状腺降钙素mRNA水平显着上调。（笑声）。

GLP-1RAs and Osteoblasts Osteoblasts arise through the differentiation of mesenchymal stem cells and play a crucial role in the process of bone formation. Stimulating GLP-1R in BMSCs triggers the buildup of nuclear β-catenin, which, in turn, activates osteogenic genes by binding with TCF7L12.371 In osteoblasts, the administration of GLP-1 and GIP incretins suppressed the excessive expression of the pro-degradative enzymes MMP-3 and MMP-13 induced by IL-1β stimulation.372 In vitro, GLP-1 disrupts the ability of osteoblasts to survive and differentiate by triggering the activation of c-Fos, which is a proto-oncogene.373 In fact, when BMSCs are exposed to exendin-4, the expression of genes related to bone development factors such as Runx and Osterix, as well as genes responsible for producing the bone matrix such as Balp and Bglap, is upregulated.

GLP-1RAs和成骨细胞成骨细胞通过间充质干细胞的分化而产生，并在骨形成过程中起关键作用。刺激骨髓间充质干细胞中的GLP-1R会触发核β-连环蛋白的积累，进而通过与成骨细胞中的TCF7L12.371结合来激活成骨基因，GLP-1和GIP肠促胰岛素的施用抑制了IL-1β刺激诱导的促降解酶MMP-3和MMP-13的过度表达。372在体外，GLP-1通过触发c-Fos（一种原癌基因）的激活来破坏成骨细胞的存活和分化能力。事实上，当骨髓间充质干细胞暴露于exendin-4时，与骨发育因子相关的基因的表达，例如Runx和Osterix以及负责产生骨基质的基因（例如Balp和Bglap）被上调。

Moreover, stimulation of GLP-1R in BMSCs results in the accumulation of β-catenin in the cell nucleus. This accumulation facilitates the binding of β-catenin to TCF7L12, triggering the activation of genes associated with osteogenesis.371.

此外，BMSCs中GLP-1R的刺激导致β-连环蛋白在细胞核中的积累。这种积累促进了β-连环蛋白与TCF7L12的结合，触发了与成骨相关的基因的激活。

In a study examining the effects of GLP-1RA on osteoporosis induced by ovariectomy in aged rats, administering exendin-4 for 16 weeks prevented deterioration of the trabecular microarchitecture and increased bone strength. This was achieved by inhibiting bone resorption through an increase in the OPG/RANKL ratio and promoting bone formation by enhancing the expression of osteoblast-specific transcription factors.374 Exendin-4 has also been shown to stimulate osteoblast activity and mitigate bone loss in an ovariectomized mouse model.374 Liraglutide can directly enhance bone formation in the MC3T3-E1 osteoblastic cell line.

在一项研究GLP-1RA对老年大鼠卵巢切除术引起的骨质疏松症的影响的研究中，给予exendin-4 16周可防止小梁微结构的恶化和骨强度的增加。这是通过增加OPG/RANKL比率来抑制骨吸收，并通过增强成骨细胞特异性转录因子的表达来促进骨形成.374 Exendin-4也被证明可以刺激成骨细胞活性并减轻去卵巢小鼠模型中的骨丢失.374利拉鲁肽可以直接增强MC3T3-E1成骨细胞系中的骨形成。

This effect is achieved through the activation of signaling pathways such as the ERK1/2, PI3K/AKT, and cAMP/PKA/β-cat-Ser675 pathways, which are mediated by GLP-1RAs.375 (Fig. 3).Fig. 3The Effects of GLP-1RAs on osteoclasts and osteoblasts. GLP-1RAs aid in weight loss by regulating the gut-brain axis and interacting with leptin, while weight loss can alleviate the harmful effects of obesity on the body, particularly in knee OA, by reducing joint loading and inflammation.

这种效应是通过激活信号通路如ERK1/2，PI3K/AKT和cAMP/PKA/β-cat-Ser675通路来实现的，这些通路由GLP-1RAs.375介导（图3）。图3 GLP-1RAs对破骨细胞和成骨细胞的影响。GLP-1RAs通过调节肠脑轴并与瘦素相互作用来帮助减肥，而减肥可以通过减少关节负荷和炎症来减轻肥胖对身体的有害影响，特别是在膝关节OA中。

Obesity disrupts bone metabolism and leads to increased bone resorption, but GLP-1RAs can inhibit this damage and improve bone health by increasing the OPG/RANKL ratio, reducing osteoclast activity, and promoting bone formationFull size image.

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GLP-1RAs and muscle

GLP-1RAs和肌肉

GLP-1RAs and Muscle Atrophy In previous experiments, exendin-4 (Ex-4) inhibited the expression of myostatin (MSTN), atrophy-factor F-box only protein 32 (atrogin-1) and muscle ring finger protein 1 (MuRF-1) in dexamethasone-treated C2C12 myotubes.376,377,378 In a dexamethasone-induced muscle atrophy model, Ex-4 ameliorated muscle atrophy by inhibiting muscle atrophy factor and enhancing myogenic factors (MyoG and MyoD), thereby increasing muscle mass and function.

GLP-1RAs和肌肉萎缩在先前的实验中，exendin-4（Ex-4）抑制地塞米松处理的C2C12肌管中肌肉生长抑制素（MSTN），萎缩因子F-box-only蛋白32（atrogin-1）和肌肉无名指蛋白1（MuRF-1）的表达。在地塞米松诱导的肌肉萎缩模型中，Ex-4通过抑制肌肉萎缩因子和增强肌源性因子（MyoG和MyoD）来改善肌肉萎缩，从而增加肌肉质量和功能。

In the muscle atrophy mouse model, Ex-4 also increased muscle mass and muscle fiber size and improved muscle function. In addition, treatment with the long-acting GLP-1RA duraglutide restored muscle mass and function in DBA/2J-mdx mice.379.

在肌肉萎缩小鼠模型中，Ex-4还增加了肌肉质量和肌纤维大小，并改善了肌肉功能。此外，长效GLP-1RA duraglutide治疗可恢复DBA/2J mdx小鼠的肌肉质量和功能。

GLP-1RAs, particularly PF1801, have demonstrated effective relief in inflammatory myopathies, such as polymyositis (PM), through preclinical studies.376,380 The therapeutic effects of PF1801 are primarily achieved by modulating several key proteins that play central roles in inflammation and cellular metabolism.380 Firstly, the expression of GLP-1R is enhanced in the inflamed muscle fibers under pathological conditions, revealing the critical role of GLP-1R in regulating the muscle’s response to inflammation.381 PF1801 activates these receptors, initiating a series of biological responses that influence the inflammatory state of muscle cells, thereby alleviating inflammation.

GLP-1RAs，特别是PF1801，通过临床前研究已经证明可以有效缓解炎症性肌病，如多发性肌炎（PM）。376380 PF1801的治疗效果主要是通过调节几种在炎症和细胞代谢中起核心作用的关键蛋白来实现的。首先，GLP-1R的表达在病理条件下在发炎的肌纤维中增强，揭示了GLP-1R在调节肌肉对炎症反应中的关键作用。381 PF1801激活这些受体，引发一系列影响肌肉细胞炎症状态的生物反应，从而减轻炎症。

Next, PF1801 exerts its effects by activating AMP-activated protein kinase (AMPK).382 As a central node in energy sensing and metabolic regulation, the activation of AMPK helps maintain cellular energy balance and prevents cell death due to energy depletion.383,384 Importantly, the activation of AMPK reduces the expression of phosphoglycerate mutase 5 (PGAM5), which plays a promotive role in cell necrosis by contributing to mitochondrial dysfunction and the production of reactive oxygen species (ROS).385,386,387 Thus, by inhibiting PGAM5, AMPK suppresses necrosis, reduces ROS accumulation, and mitigates oxidative stress.385,387 PF1801 displays its anti-inflammatory effects by lowering levels of inflammatory mediators such as TNFα, IL-6, and HMGB1, and enhances the cell’s antioxidant capability by upregulating molecules like Nfe2l2, Hmox1, Gclm, and Nqo1, which further improves cellular defense against oxidative stress and protects them from further damage.382 Through this sophisticated molecular regulation, PF1801 not only alleviates inflammation and necrosis in muscle fibers but also enhances the .

接下来，PF1801通过激活AMP激活的蛋白激酶（AMPK）发挥其作用。382作为能量感应和代谢调节的中心节点，AMPK的激活有助于维持细胞能量平衡并防止由于能量消耗而导致的细胞死亡。383384重要的是，AMPK的激活降低了磷酸甘油酸突变酶5（PGAM5）的表达，磷酸甘油酸突变酶5（PGAM5）通过促进线粒体功能障碍和活性氧（ROS）的产生而在细胞坏死中发挥促进作用。385386387因此，AMPK通过抑制PGAM5来抑制坏死，减少ROS的积累，减轻氧化应激。385387 PF1801通过降低炎症介质的水平来显示其抗炎作用，例如作为TNFα，IL-6和HMGB1，并通过上调Nfe2l2，Hmox1，Gclm和Nqo1等分子来增强细胞的抗氧化能力，这进一步提高了细胞对氧化应激的防御能力，并保护它们免受进一步的损伤.382通过这种复杂的分子调控，PF1801不仅减轻了肌纤维的炎症和坏死，而且增强了肌纤维的炎症和坏死。

GLP-1RAs in Enhancing Exercise Endurance Studies indicate that acute exercise and short-term endurance training significantly increase GLP-1 secretion in mice. In endurance-trained men, GLP-1 plasma concentrations are elevated immediately at 30 and 45 minutes after exercise.388 To confirm the role of GLP-1 in enhancing physical endurance and the possible mechanisms involved, an in vivo AAV-mediated GLP-1 overexpression model and an in vitro siRNA-mediated AMPK knockdown model were generated.

GLP-1RAs在增强运动耐力方面的研究表明，急性运动和短期耐力训练显着增加了小鼠GLP-1的分泌。在耐力训练的男性中，GLP-1血浆浓度在运动后30分钟和45分钟立即升高.388为了证实GLP-1在增强身体耐力中的作用及其可能的机制，产生了体内AAV介导的GLP-1过表达模型和体外siRNA介导的AMPK敲低模型。

We demonstrated that GLP-1 enhances physical endurance by inducing skeletal muscle remodeling, which may be mediated by GLP-1R/AMPK signaling.389 Overall, GLP-1 secretion is induced by exercise. Overexpression of GLP-1 in skeletal muscle can improve endurance. These results suggest that GLP-1 may improve exercise endurance in mice by enhancing skeletal muscle glycogen synthesis and glucose uptake.

我们证明GLP-1通过诱导骨骼肌重塑来增强身体耐力，这可能是由GLP-1R/AMPK信号传导介导的.389总体而言，GLP-1分泌是由运动诱导的。骨骼肌中GLP-1的过度表达可以提高耐力。这些结果表明，GLP-1可能通过增强骨骼肌糖原合成和葡萄糖摄取来改善小鼠的运动耐力。

Mitochondrial content and function in skeletal muscle are regulated by GLP-1.389 The interaction between GLP-1 and its receptor GLP-1R initiates the AMPK signaling cascade within skeletal muscle tissue. This initiation precipitates a multitude of alterations in the cellular milieu, notably the augmentation of mitochondrial biogenesis-a mechanism responsible for the genesis of new mitochondria.

骨骼肌中的线粒体含量和功能受GLP-1.389调节。GLP-1及其受体GLP-1R之间的相互作用启动骨骼肌组织内的AMPK信号级联反应。这种启动促使细胞环境发生多种变化，特别是线粒体生物发生的增加，这是导致新线粒体发生的机制。

Furthermore, GLP-1 augments mitochondrial efficacy, as manifested by the ameliorated oxidative metabolism of muscle tissue. This enhancement is demonstrable through an increase in mitochondrial DNA content, the upregulation of genes integral to mitochondrial biogenesis, and the increased expression of proteins pivotal in oxidative phosphorylation.

此外，GLP-1增强线粒体功效，表现为肌肉组织的氧化代谢得到改善。这种增强可以通过线粒体DNA含量的增加，线粒体生物发生不可或缺的基因的上调以及氧化磷酸化关键蛋白的表达增加来证明。

These cellular transformations contribute significantly to enhanced endurance during exercise, thereby underscoring the critical role that GLP-1 plays in t.

这些细胞转化显着提高了运动期间的耐力，从而强调了GLP-1在t中的关键作用。

GLP-1RAs and fat metabolismGLP-1RAs work via numerous mechanisms that contribute to weight loss, one of the most well-known of which is the gut-brain axis.212,213,390 Within this axis, GLP-1 functions by acting on both the gut and the brain.391 Furthermore, the combination of GLP-1-mediated signaling and the adipocyte hormone leptin has recently garnered increased interest.

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Notably, leptin may serve as a crucial biological signal for GLP-1, working in synergy, to decrease food intake and body weight. The effects of the leptin-GLP-1 interaction may be governed by intracellular signaling pathways, including those involving phosphorylated STAT3 and PTP1B.15,392In Wistar rats, a diet high in fat was found to lead to a decrease in the ratio of OPG/RANKL, which resulted in increased bone resorption and ultimately a reduction in bone mass.

值得注意的是，瘦素可能是GLP-1的关键生物信号，协同作用，减少食物摄入和体重。瘦素-GLP-1相互作用的影响可能受细胞内信号通路的控制，包括涉及磷酸化STAT3和PTP1B的信号通路。15392在Wistar大鼠中，发现高脂肪饮食导致OPG/RANKL比例降低，导致骨吸收增加，最终骨量减少。

The administration of GLP-1RA or exendin-4 to rats fed a high-fat diet resulted in an increase in the OPG/RANKL ratio and a reduction in the degree of bone loss. It was observed that the treatment of rats on a high-fat diet with exendin-4 resulted in a decrease in the number of osteoclasts and the area of eroded surfaces, while there was an increase in the osteoid area, bone mass, and trabecular bone volume.

向喂食高脂饮食的大鼠施用GLP-1RA或exendin-4导致OPG/RANKL比率增加和骨质流失程度降低。据观察，用exendin-4治疗高脂饮食的大鼠导致破骨细胞数量和侵蚀表面面积减少，而类骨质面积，骨量和骨小梁体积增加。

These effects were compared to those of untreated controls that were also maintained on a high-fat diet.393 As a result, GLP-1RAs could mitigate the detrimental effects of hyperlipidemia-induced skeletal defects, leading to an improved prognosis in individuals with OA.On the surface of the cartilage, there is a layer of special phospholipids.

这些影响与未经治疗的对照组进行了比较，这些对照组也维持在高脂饮食中.393因此，GLP-1RAs可以减轻高脂血症引起的骨骼缺陷的有害影响，从而改善OA患者的预后。软骨表面有一层特殊的磷脂。

When a joint bears weight, it functions as a lubricant, playing a crucial role in enabling the joint to continue operating efficiently and smoothly. Altering the composition of this phospholipid lay.

当关节承受重量时，它起着润滑剂的作用，在使关节继续高效平稳地工作中起着至关重要的作用。改变这种磷脂层的组成。

Hepatocellular carcinoma (HCC)

肝细胞癌（HCC）

Initially developed for treating diabetes, GLP-1RAs have shown potential in treating NASH, which is closely related to HCC.513 Studies suggest that the anti-inflammatory and metabolic effects of GLP-1RAs might also influence the progression of liver diseases, including HCC.503,512,518 These effects include modulating cell proliferation, inflammation, and oxidative stress in liver cells, all of which are key factors in the development and progression of HCC.513,522 In a mouse model induced with NASH-related HCC, treatment with liraglutide (a type of GLP-1RA) was shown to prevent the progression of hepatocellular carcinoma.518 This was observed through improved glycemic control, reduced occurrence of liver cancer, and better liver histology compared to the control group.518 Studies indicate that liraglutide may inhibit liver carcinogenesis through its metabolic effects, suggesting that GLP-1RAs could potentially play a role in preventing or managing HCC in the context of NASH.523 Not only hepatocellular carcinoma, but GLP-1 has also shown potential in the treatment of other gastrointestinal tumors.524,525.

最初开发用于治疗糖尿病的GLP-1RAs已显示出治疗NASH的潜力，NASH与HCC密切相关.513研究表明，GLP-1RAs的抗炎和代谢作用也可能影响肝脏疾病的进展，包括HCC.503512518这些作用包括调节肝细胞的细胞增殖，炎症和氧化应激，所有这些都是HCC发展和进展的关键因素.513522在NASH相关HCC诱导的小鼠模型中，利拉鲁肽（一种GLP-1RA）的治疗被证明可以预防肝细胞癌的进展.518这是通过改善血糖控制，减少肝癌的发生而观察到的。518研究表明，利拉鲁肽可能通过其代谢作用抑制肝癌的发生，提示GLP-1RAs可能在NASH的背景下预防或管理HCC中发挥作用[523]。不仅肝细胞癌，GLP-1也显示出治疗其他胃肠道肿瘤的潜力[524525]。

Pancreatic cancer

胰腺癌

Researchers first compared the expression of GLP-1R in human pancreatic cancer tissues with adjacent non-tumorous pancreatic tissues, finding generally lower or absent expression of GLP-1R in pancreatic cancer tissues.520 Subsequently, the study observed that treatment with liraglutide, both in vitro (cell culture models) and in vivo (mouse models), inhibited the tumor formation and metastatic capabilities of pancreatic cancer cells by activating GLP-1R.520 The anti-tumor effect of liraglutide is related to its inhibition of the PI3K/Akt signaling pathway, as the activation of Akt is crucial for promoting cell survival and proliferation, and liraglutide can inhibit this process in a dose-dependent manner.520,526 In the context of T2DM, liraglutide, by regulating the PI3K/Akt pathway and activating GLP-1R, effectively inhibits the growth and spread of pancreatic cancer cells.520.

研究人员首先比较了GLP-1R在人胰腺癌组织和邻近的非肿瘤性胰腺组织中的表达，发现GLP-1R在胰腺癌组织中的表达通常较低或不存在。随后，该研究观察到利拉鲁肽在体外（细胞培养模型）和体内（小鼠模型）通过激活GLP-1R抑制胰腺癌细胞的肿瘤形成和转移能力。利拉鲁肽的抗肿瘤作用与其抑制PI3K/Akt信号通路有关，因为Akt的激活对于促进细胞存活和增殖至关重要，利拉鲁肽可以剂量依赖性方式抑制这一过程。520526在T2DM的背景下，利拉鲁肽通过调节PI3K/Akt途径和激活GLP-1R，有效抑制胰腺癌细胞的生长和扩散。

Colorectal cancer

大肠癌

The potential impact of GLP-1RAs on colorectal cancer (CRC) treatment is achieved through the modulation of Bone Morphogenetic Protein 4 (BMP4).519 In T2DM and CRC, the regulation of BMP4 is abnormal, which is a key focus of the research.519 Specifically, high blood glucose-induced insulin resistance in CRC cells leads to increased BMP4 expression, which activates the BMP4-Smad1/5/8 signaling pathway.519 The activation of this pathway enhances cell proliferation and metastatic capabilities by promoting epithelial-mesenchymal transition (EMT), thereby increasing the invasiveness and metastatic potential of tumors.

GLP-1RAs对结直肠癌（CRC）治疗的潜在影响是通过调节骨形态发生蛋白4（BMP4）来实现的。在T2DM和CRC中，BMP4的调节异常，这是研究的重点。具体而言，高血糖诱导的CRC细胞胰岛素抵抗导致BMP4表达增加，从而激活BMP4-Smad1/5/8信号通路。该通路的激活通过促进上皮-间质转化（EMT）增强细胞增殖和转移能力，从而增加肿瘤的侵袭性和转移潜能。

However, GLP-1RAs have been shown to reduce BMP4 levels through exogenous administration. Studies have shown that treating CRC cells with GLP-1RA can inhibit cell proliferation induced by insulin resistance by downregulating BMP4. Therefore, BMP4 becomes a potential therapeutic target in CRC, especially in a diabetic context where high blood glucose significantly affects cancer progression through the BMP4 pathway.519 Ultimately, GLP-1RA, by regulating BMP4 and its effects on cell proliferation and metastasis, provides a promising treatment approach.519 This not only demonstrates the role of GLP-1RA in diabetes management but also offers potential for integrating diabetes and cancer treatment.520 This finding emphasizes the importance of considering metabolic status in cancer treatment and the necessity for further research in this area.519 While early models have shown promising results, the application of GLP-1RAs in cancer treatment has not yet been established and requires further clinical trials.527.

然而，已显示GLP-1RAs通过外源给药降低BMP4水平。研究表明，用GLP-1RA处理CRC细胞可以通过下调BMP4来抑制胰岛素抵抗诱导的细胞增殖。因此，BMP4成为CRC的潜在治疗靶点，特别是在高血糖通过BMP4途径显着影响癌症进展的糖尿病背景下.519最终，GLP-1RA通过调节BMP4及其对细胞增殖和转移的影响，提供了一种有希望的治疗方法.519这不仅证明了GLP-1RA在糖尿病管理中的作用，而且为整合糖尿病和癌症治疗提供了潜力.520这一发现强调了在癌症治疗中考虑代谢状态的重要性以及在这一领域进一步研究的必要性.519虽然早期模型已显示出有希望的结果，但GLP-1RAs在癌症治疗中的应用尚未建立，需要进一步的临床试验.527是的。

Conclusions and perspectivePrimarily recognized for their role in diabetes mellitus treatment, GLP-1RAs have demonstrated significant benefits in cardiovascular health, skeletal muscle-related diseases, obesity management, and neurodegenerative conditions, among others. In this review, we delved into the multifaceted role of GLP-1R, especially its significance in disease contexts beyond traditional glucose metabolism.

结论和观点GLP-1RAs主要因其在糖尿病治疗中的作用而被认可，在心血管健康，骨骼肌相关疾病，肥胖管理和神经退行性疾病等方面显示出显着的益处。在这篇综述中，我们深入研究了GLP-1R的多方面作用，特别是其在传统葡萄糖代谢以外的疾病背景下的意义。

It explored the mechanisms of action of GLP-1RAs and their therapeutic potential in a wide array of diseases, such as diabetes mellitus, providing new insights into metabolic disease management. These findings underscore the multifunctionality of GLP-1R as a therapeutic target and its involvement in various biological processes, emphasizing its role in addressing complex disease mechanisms.

。这些发现强调了GLP-1R作为治疗靶标的多功能性及其参与各种生物学过程，强调了其在解决复杂疾病机制中的作用。

GLP-1 acts on the GLP-1R, activating multiple intracellular signaling pathways, including the cAMP/PKA pathway, the PI3K/Akt signaling pathway, and pathways related to anti-inflammatory and anti-oxidative stress responses, among others. These pathways play a crucial role in its wide-ranging therapeutic effects, extending the benefits of GLP-1RAs beyond metabolic diseases.

GLP-1作用于GLP-1R，激活多种细胞内信号传导途径，包括cAMP/PKA途径，PI3K/Akt信号传导途径以及与抗炎和抗氧化应激反应相关的途径等。这些途径在其广泛的治疗效果中起着至关重要的作用，将GLP-1RAs的益处扩展到代谢疾病之外。

While the therapeutic benefits of GLP-1RAs in diabetes management are well-established, their emerging role in other diseases suggests novel treatment strategies. Conclusively, research on GLP-1R and its agonists marks a promising direction in metabolic disease therapy, extending their potential beyond glucose regulation and offering hope for more comprehensive approaches in addressing metabolic diseases.

虽然GLP-1RAs在糖尿病管理中的治疗益处已经确立，但它们在其他疾病中的新兴作用提示了新的治疗策略。总之，对GLP-1R及其激动剂的研究标志着代谢疾病治疗的一个有希望的方向，将其潜力扩展到葡萄糖调节之外，并为解决代谢疾病的更全面方法提供了希望。

This research necessitates continued exploration, potentially revolutionizing future therapeutic strategies.In the intensely competitive GLP-1 drug market, simply enhancing drug efficacy is no longer .

这项研究需要继续探索，可能会彻底改变未来的治疗策略。在竞争激烈的GLP-1药物市场中，不再简单地提高药物疗效。

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Download referencesAcknowledgementsThis study was performed with the support of the National Natural Science Foundation of China (82002339, 81820108020), Shanghai Frontiers Science Center of Degeneration and Regeneration in Skeletal System (BJ1-9000-22-4002). BioRender (https://www.biorender.com/) was used to create the Fig.

下载参考文献致谢本研究得到了国家自然科学基金（8200233981820108200），上海骨骼系统退化与再生前沿科学中心（BJ1-9000-22-4002）的支持。BioRender公司(https://www.biorender.com/)被用来创建Fig。

2.Author informationAuthor notesThese authors contributed equally: Zhikai Zheng, Yao ZongAuthors and AffiliationsDepartment of Orthopaedics, Shanghai Sixth People’s Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, 200233, ChinaZhikai Zheng, Yiyang Ma, Yucheng Tian, Yidan Pang, Changqing Zhang & Junjie GaoInstitute of Microsurgery on Extremities, and Department of Orthopedic Surgery, Shanghai Sixth People’s Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, 200233, ChinaZhikai Zheng, Yiyang Ma, Yucheng Tian, Yidan Pang, Changqing Zhang & Junjie GaoCentre for Orthopaedic Research, Medical School, The University of Western Australia, Nedlands, WA, 6009, AustraliaYao ZongAuthorsZhikai ZhengView author publicationsYou can also search for this author in.

2.作者信息作者注意到，这些作者做出了同样的贡献：郑志凯，姚宗浩及其附属医院上海交通大学医学院附属上海第六人民医院骨科，上海，200233，中国郑志凯，马益阳，田玉成，彭义丹，张长庆和高俊杰四肢显微外科研究所，上海交通大学医学院附属上海第六人民医院骨科，上海，200233，中国郑志凯，马益阳，田玉成，彭义丹，张长庆和高俊杰骨科研究中心西澳大利亚大学医学院，内德兰兹，华盛顿州，6009，澳大利亚Ayao ZongAuthorsZhikai ZhengView作者出版物您也可以在中搜索这位作者。

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PubMed Google ScholarContributionsZ.Z., Y.Z. and J.G. drafted and conceived the initial manuscript. J.G. and C.Z. provided the essential assistant for our final manuscript. Z.Z., Y.M., Y.T., Y.Z. and Y.P. drew the figures and arranged the tables. All authors have read and approved the article.Corresponding authorCorrespondence to.

PubMed谷歌学术贡献。Z、 ，Y.Z.和J.G.起草并构思了初稿。J、 G.和C.Z.为我们的最终手稿提供了必不可少的助手。Z、 Z.，Y.M.，Y.T.，Y.Z.和Y.P.绘制了数字并安排了表格。。对应作者对应。

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