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糖尿病肾病中的管状损伤:分子机制和潜在的治疗前景。

Tubular injury in diabetic kidney disease: molecular mechanisms and potential therapeutic perspectives.

机构信息

Department of Endocrinology and Metabolism, Shenzhen University General Hospital, Shenzhen, Guangdong, China.

Department of Biomedical Sciences, City University of Hong Kong, Hong Kong, Hong Kong SAR, China.

出版信息

Front Endocrinol (Lausanne). 2023 Aug 2;14:1238927. doi: 10.3389/fendo.2023.1238927. eCollection 2023.

DOI:10.3389/fendo.2023.1238927
PMID:37600689
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10433744/
Abstract

Diabetic kidney disease (DKD) is a chronic complication of diabetes and the leading cause of end-stage renal disease (ESRD) worldwide. Currently, there are limited therapeutic drugs available for DKD. While previous research has primarily focused on glomerular injury, recent studies have increasingly emphasized the role of renal tubular injury in the pathogenesis of DKD. Various factors, including hyperglycemia, lipid accumulation, oxidative stress, hypoxia, RAAS, ER stress, inflammation, EMT and programmed cell death, have been shown to induce renal tubular injury and contribute to the progression of DKD. Additionally, traditional hypoglycemic drugs, anti-inflammation therapies, anti-senescence therapies, mineralocorticoid receptor antagonists, and stem cell therapies have demonstrated their potential to alleviate renal tubular injury in DKD. This review will provide insights into the latest research on the mechanisms and treatments of renal tubular injury in DKD.

摘要

糖尿病肾病(DKD)是糖尿病的一种慢性并发症,也是全球范围内导致终末期肾病(ESRD)的主要原因。目前,针对 DKD 的治疗药物有限。虽然之前的研究主要集中在肾小球损伤上,但最近的研究越来越强调肾小管损伤在 DKD 发病机制中的作用。多种因素,包括高血糖、脂质积累、氧化应激、缺氧、RAAS、内质网应激、炎症、EMT 和程序性细胞死亡,已被证明可诱导肾小管损伤,并促进 DKD 的进展。此外,传统的降血糖药物、抗炎治疗、抗衰老治疗、盐皮质激素受体拮抗剂和干细胞治疗已显示出缓解 DKD 肾小管损伤的潜力。本综述将深入探讨 DKD 肾小管损伤的机制和治疗的最新研究进展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d06/10433744/0ca420f1693c/fendo-14-1238927-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d06/10433744/e58320d2c1b0/fendo-14-1238927-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d06/10433744/0ca420f1693c/fendo-14-1238927-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d06/10433744/e58320d2c1b0/fendo-14-1238927-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d06/10433744/0ca420f1693c/fendo-14-1238927-g002.jpg

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