慢性肾脏病炎症和纤维化交叉路口的代谢-动脉网

Metabolism at the crossroads of inflammation and fibrosis in chronic kidney disease

Nature 等信源发布 2024-09-17 01:16

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AbstractChronic kidney disease (CKD), defined as persistent (>3 months) kidney functional loss, has a growing prevalence (>10% worldwide population) and limited treatment options. Fibrosis driven by the aberrant accumulation of extracellular matrix is the final common pathway of nearly all types of chronic repetitive injury in the kidney and is considered a hallmark of CKD.

摘要慢性肾病（CKD）定义为持续性（>3个月）肾功能丧失，其患病率越来越高（>10%的全球人口），治疗选择有限。由细胞外基质异常积累驱动的纤维化是几乎所有类型的肾脏慢性重复性损伤的最终共同途径，被认为是CKD的标志。

Myofibroblasts are key extracellular matrix-producing cells that are activated by crosstalk between damaged tubules and immune cells. Emerging evidence indicates that metabolic alterations are crucial contributors to the pathogenesis of kidney fibrosis by affecting cellular bioenergetics and metabolite signalling.

肌成纤维细胞是产生细胞外基质的关键细胞，其被受损小管和免疫细胞之间的串扰激活。新出现的证据表明，代谢改变通过影响细胞生物能学和代谢物信号传导而成为肾纤维化发病机制的关键因素。

Immune cell functions are intricately connected to their metabolic characteristics, and kidney cells seem to undergo cell-type-specific metabolic shifts in response to damage, all of which can determine injury and repair responses in CKD. A detailed understanding of the heterogeneity in metabolic reprogramming of different kidney cellular subsets is essential to elucidating communication processes between cell types and to enabling the development of metabolism-based innovative therapeutic strategies against CKD.Key points.

免疫细胞的功能与其代谢特征密切相关，肾细胞似乎会因损伤而发生细胞类型特异性代谢变化，所有这些都可以确定CKD的损伤和修复反应。详细了解不同肾脏细胞亚群代谢重编程的异质性对于阐明细胞类型之间的通讯过程以及开发基于代谢的针对CKD的创新治疗策略至关重要。关键点。

The kidney has distinctive anatomical and physiological characteristics, and kidney cell types have specialized metabolic traits tailored to their specific functions and location.

肾脏具有独特的解剖学和生理学特征，肾细胞类型具有针对其特定功能和位置量身定制的特殊代谢特征。

In general, all kidney cells — including epithelial, endothelial, stromal and immune cells — can have an impact on fibrosis, and their roles are determined by spatiotemporal metabolic reprogramming that coordinates their effector functions and interactions.

一般来说，所有肾细胞-包括上皮细胞，内皮细胞，基质细胞和免疫细胞-都可以对纤维化产生影响，它们的作用是通过时空代谢重编程来确定的，这些重编程可以协调它们的效应功能和相互作用。

Identification of cell-type-specific metabolic shifts could enable the recognition of novel cell subpopulations with distinctive roles in adaptive or fibrotic kidney regeneration.

鉴定细胞类型特异性代谢变化可以识别在适应性或纤维化肾再生中具有独特作用的新细胞亚群。

Targeting metabolic routes and energy-sensing molecules to promote an immune anti-inflammatory or quiescent state might avoid chronic inflammation and subsequent development of kidney fibrosis.

靶向代谢途径和能量感应分子以促进免疫抗炎或静止状态可能会避免慢性炎症和随后的肾纤维化发展。

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Fig. 1: Cellular crosstalk in the pathological progression of kidney fibrosis.Fig. 2: Main pathways of cellular metabolism involved in kidney fibrogenesis.Fig. 3: Metabolic alterations in tubular epithelial cells contributing to kidney fibrogenesis.Fig. 4: Metabolomic reprogramming of endothelial cells, podocytes and myofibroblasts..

图1：肾纤维化病理进展中的细胞串扰。图2：参与肾纤维化的细胞代谢的主要途径。。图4：内皮细胞，足细胞和肌成纤维细胞的代谢组学重编程。。

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Download referencesAcknowledgementsThis work was supported by grants from the German Research Foundation (DFG: SFBTRR219) CRU344 4288578857858 and CRU5011 445703531, a grant from the Else Kroener Fresenius Foundation, the Dutch Kidney Foundation TASKFORCE EP1805 and Kolff Grant #113351, the Leducq Foundation, the BMBF eMed Consortia Fibromap and the BMBF Consortia CureFib to R.K.

下载参考文献致谢这项工作得到了德国研究基金会（DFG:SFBTRR219）CRU344 4288578857858和CRU5011 445703531的资助，这是Else Kroener Fresenius基金会，荷兰肾脏基金会特别工作组EP1805和Kolf grant#113351，Leducq基金会，BMBF eMed Consortia Fibromap和BMBF Consortia CureFib授予R.K的资助。

V.M. was supported by a FEBS Long-Term Fellowship. I.W.S. is funded by a Benjamin Hochberg Fellowship from the DFG.Author informationAuthors and AffiliationsDepartment of Medicine 2, Nephrology, Rheumatology and Immunology, RWTH Aachen University, Medical Faculty, Aachen, GermanyVerónica Miguel, Isaac W.

五、 M.得到了FEBS长期奖学金的支持。一、 W.S.由DFG的Benjamin Hochberg奖学金资助。作者信息作者和附属机构亚琛RWTH大学医学院肾脏病，风湿病和免疫学2系，亚琛医学院，GermanyVerónica Miguel，Isaac W。

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相互竞争的利益

R.K. is founder and shareholder of Sequantrix GmbH, has grants from Travere Therapeutics, Galapagos, Chugai, AskBio and Novo Nordisk, and is a consultant for Bayer, Pfizer, Novo Nordisk, Hybridize Therapeutics and Gruenenthal. The other authors declare no competing interests.

R、 K.是Sequantrix GmbH的创始人和股东，拥有Travere Therapeutics，Galapagos，Chugai，AskBio和Novo Nordisk的资助，是拜耳，辉瑞，Novo Nordisk，Hybridize Therapeutics和Gruenenthal的顾问。其他作者声明没有利益冲突。

Peer review

同行评审

Peer review information

同行评审信息

Nature Reviews Nephrology thanks Sandeep Mallipattu, Alessandra Tammaro, Liu Ye and the other, anonymous, reviewer(s) for their contribution to the peer review of this work.

《自然评论肾脏病学》感谢Sandeep Mallipattu，Alessandra Tammaro，Liu Ye和另一位匿名审稿人对这项工作的同行评审做出的贡献。

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Additional informationPublisher的注释Springer Nature在已发布地图和机构隶属关系中的管辖权主张方面保持中立。权利和许可Pringer Nature或其许可人（例如协会或其他合作伙伴）根据与作者或其他权利持有人的出版协议对本文拥有专有权；本文接受稿件版本的作者自行存档仅受此类出版协议和适用法律的条款管辖。转载和许可本文引用本文Miguel，V.，Shaw，I.W。

& Kramann, R. Metabolism at the crossroads of inflammation and fibrosis in chronic kidney disease..

&Kramann，R。慢性肾脏病炎症和纤维化十字路口的代谢。。

Nat Rev Nephrol (2024). https://doi.org/10.1038/s41581-024-00889-zDownload citationAccepted: 15 August 2024Published: 17 September 2024DOI: https://doi.org/10.1038/s41581-024-00889-zShare this articleAnyone you share the following link with will be able to read this content:Get shareable linkSorry, a shareable link is not currently available for this article.Copy to clipboard.

Nat Rev Nephrol（2024年）。https://doi.org/10.1038/s41581-024-00889-zDownload引文接受日期：2024年8月15日发布日期：2024年9月17日OI：https://doi.org/10.1038/s41581-024-00889-zShare本文与您共享以下链接的任何人都可以阅读此内容：获取可共享链接对不起，本文目前没有可共享的链接。复制到剪贴板。

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