AbstractOne of the main characteristics of diabetic kidney disease (DKD) is abnormal renal tubular fatty acid metabolism, especially defective fatty acid oxidation (FAO), accelerating tubular injury and tubulointerstitial fibrosis. Thiosulfate sulfurtransferase (TST), a mitochondrial enzyme essential for sulfur transfer, is reduced in metabolic diseases like diabetes and obesity.

摘要糖尿病肾病（DKD）的主要特征之一是肾小管脂肪酸代谢异常，尤其是脂肪酸氧化缺陷（FAO），加速肾小管损伤和肾小管间质纤维化。硫代硫酸盐硫转移酶（TST）是一种对硫转移至关重要的线粒体酶，在糖尿病和肥胖症等代谢疾病中会减少。

However, the potential role of TST in regulating fatty acid metabolic abnormalities in DKD remains unclear. Here, our data revealed decreased TST expression in the renal cortex of DKD patients. TST deficiency exacerbated tubular impairment in both diabetic and renal fibrosis mouse models, while sodium thiosulfate treatment or TST overexpression mitigated renal tubular injury with high-glucose exposure.

然而，TST在调节DKD脂肪酸代谢异常中的潜在作用仍不清楚。在这里，我们的数据显示DKD患者肾皮质中TST表达降低。TST缺乏加剧了糖尿病和肾纤维化小鼠模型中的肾小管损伤，而硫代硫酸钠治疗或TST过表达减轻了高糖暴露下的肾小管损伤。

TST downregulation mediated the decrease in S-sulfhydration of very long-chain specific acyl-CoA dehydrogenase, resulting in mitochondrial FAO dysfunction. This sequence of events exacerbates the progression of tubulointerstitial injury in DKD. Together, our findings demonstrate TST as a regulator of renal tubular injury in DKD..

TST下调介导了超长链特异性酰基辅酶A脱氢酶S-磺酰化的减少，导致线粒体FAO功能障碍。这一系列事件加剧了DKD肾小管间质损伤的进展。总之，我们的研究结果表明TST是DKD肾小管损伤的调节剂。。

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Fig. 1: TST expression was decreased in renal tubular epithelial cells of patients with DKD or in HK-2 cells exposed to high glucose.Fig. 2: Diabetic TST knockout mice worsened renal fibrosis.Fig. 3: Thiosulfate treatment protected kidneys from diabetic lesions via TST activation.Fig. 4: TST overexpression ameliorated the injury of renal tubular epithelial cells caused by high glucose.Fig.

图1:DKD患者的肾小管上皮细胞或暴露于高糖的HK-2细胞中TST表达降低。图2：糖尿病TST基因敲除小鼠加重了肾纤维化。图3：硫代硫酸盐治疗通过TST激活保护肾脏免受糖尿病病变。图4:TST过表达改善了由高糖引起的肾小管上皮细胞的损伤。图。

5: STS treatment alleviated HG-induced tubular epithelial cell dysfunction and mitochondrial damage.Fig. 6: TST maintained mitochondrial FAO homeostasis in renal tubular epithelial cells in diabetic conditions.Fig. 7: TST promoted S-sulfhydration of VLCAD..

5： STS治疗减轻了HG诱导的肾小管上皮细胞功能障碍和线粒体损伤。图6:TST在糖尿病条件下维持肾小管上皮细胞中的线粒体FAO稳态。图7:TST促进VLCAD的S-硫化。。

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我们验证作者提供了所有相关数据。我们还提交了完整和未切割的蛋白质印迹作为补充材料。

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Download referencesFundingThis study was supported by the National Natural Science Foundation of China (82170736, 81970629, 82370716), and the Natural Science Foundation of Zhejiang Province (LHDMY23H070002).Author informationAuthors and AffiliationsInstitute of Nephrology, Zhong da Hospital, School of Medicine, Southeast University, Nanjing, ChinaJia Xiu Zhang, Pei Pei Chen, Xue Qi Li, Liang Li, Qin Yi Wu, Gui Hua Wang & Kun Ling MaDepartment of Nephrology, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, ChinaPei Pei Chen & Kun Ling MaCentre for Lipid Research, Key Laboratory of Molecular Biology on Infectious Diseases, Ministry of Education, Chongqing Medical University, Chongqing, ChinaXiong Zhong RuanAuthorsJia Xiu ZhangView author publicationsYou can also search for this author in.

下载参考文献资助本研究得到了国家自然科学基金（821707368197062982370716）和浙江省自然科学基金（LHDMY23H070002）的支持。作者信息作者和附属机构南京东南大学医学院中大医院肾脏病研究所张家秀，陈培培，薛启立，梁丽，秦一武，王桂华和昆陵医学院第二附属医院肾脏病学系，浙江大学医学院，杭州，中国培培培陈和昆陵脂质研究中心，重庆医科大学教育部传染病分子生物学重点实验室，重庆，中国熊中软作者张家秀作者出版物您也可以在中搜索这位作者。

PubMed Google ScholarPei Pei ChenView author publicationsYou can also search for this author in

PubMed Google ScholarPei Pei ChenView作者出版物您也可以在

PubMed Google ScholarXue Qi LiView author publicationsYou can also search for this author in

PubMed Google ScholarXue Qi LiView作者出版物您也可以在

PubMed Google ScholarLiang LiView author publicationsYou can also search for this author in

PubMed谷歌学术Liang LiView作者出版物您也可以在

PubMed Google ScholarQin Yi WuView author publicationsYou can also search for this author in

PubMed Google ScholarQin Yi WuView作者出版物您也可以在

PubMed Google ScholarGui Hua WangView author publicationsYou can also search for this author in

PubMed Google ScholarGui Hua WangView作者出版物您也可以在

PubMed Google ScholarXiong Zhong RuanView author publicationsYou can also search for this author in

PubMed Google ScholarXiong Zhong RuanView作者出版物您也可以在

PubMed Google ScholarKun Ling MaView author publicationsYou can also search for this author in

PubMed Google ScholarKun Ling MaView作者出版物您也可以在

PubMed Google ScholarContributionsKLM and JXZ performed the study concept and design; PPC, JXZ, and XQL performed the experiments. The data were analyzed by LL, GHW, QYW; JXZ, KLM, and XZR drafted and revised the manuscript. KLM and XZR have verified the underlying data. All authors had access to the data, reviewed the manuscript, and approved the final version for submission.Corresponding authorCorrespondence to.

PubMed谷歌学术贡献SKLM和JXZ进行了研究概念和设计；PPC，JXZ和XQL进行了实验。数据由LL，GHW，QYW分析；JXZ，KLM和XZR起草并修订了手稿。KLM和XZR已经验证了基础数据。所有作者都可以访问数据，审阅稿件，并批准提交最终版本。对应作者对应。

Kun Ling Ma.Ethics declarations

马昆玲。道德宣言

Competing interests

相互竞争的利益

The authors declare no competing interests.

作者声明没有利益冲突。

Ethics approval and consent to participate

道德批准和同意参与

Animal studies were approved by the Animal Care and Use Committee of Southeast University (Approval No. 20210227025). All human studies were performed with informed patient consent and were approved from the Biomedical Ethics Committee of Zhong Da Hospital, Southeast University (Approval Number: 2019ZDSYLL057-P01).

动物研究得到东南大学动物护理和使用委员会的批准（批准号20210227025）。所有人体研究均在患者知情同意的情况下进行，并获得东南大学中大医院生物医学伦理委员会的批准（批准号：2019ZDSYLL057-P01）。

All methods were carried out in accordance with relevant guidelines and regulations..

所有方法均按照相关指南和规定进行。。

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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Zhang，J.X.，Chen，P.P.，Li，X.Q。

et al. Deficiency of thiosulfate sulfurtransferase mediates the dysfunction of renal tubular mitochondrial fatty acid oxidation in diabetic kidney disease..

硫代硫酸盐硫转移酶的缺乏介导了糖尿病肾病中肾小管线粒体脂肪酸氧化的功能障碍。。

Cell Death Differ (2024). https://doi.org/10.1038/s41418-024-01365-8Download citationReceived: 10 February 2024Revised: 11 August 2024Accepted: 14 August 2024Published: 22 August 2024DOI: https://doi.org/10.1038/s41418-024-01365-8Share 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.

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