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足细胞自噬和内质网应激在糖尿病肾病中的作用

[The role of podocyte autophagy and endoplasmic reticulum stress in diabetic kidney disease].

作者信息

Li Ruifeng, Guo Zhao'an

机构信息

Shandong University of Traditional Chinese Medicine, Jinan 250355, Shandong, China.

Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Shandong Hospital of Traditional Chinese Medicine, Jinan 250011, Shandong, China. Corresponding author: Guo Zhao'an, Email:

出版信息

Zhonghua Wei Zhong Bing Ji Jiu Yi Xue. 2022 Feb;34(2):221-224. doi: 10.3760/cma.j.cn121430-20210712-01044.

Abstract

Diabetic kidney disease (DKD) is one of the serious complications of diabetes mellitus, and it has become the leading cause of chronic renal failure in China. Podocytes are highly differentiated epithelial cells and are the important part of the glomerular filtration barrier. Apoptosis and shedding of podocytes, foot process fusion and decreased expression of slit membrane proteins can lead to proteinuria, which in turn affects the progression of DKD. Autophagy is an important process for eukaryotic cells to degrade cytoplasmic proteins and organelles,the increase of autophagy level helps to reduce podocytes damage. Endoplasmic reticulum stress (ERS) is the accumulation of misfolded proteins in cells. It allows the cells into stress state, and may be able to regulate cell damage in both directions. Autophagy and ERS are regulated by multiple signaling pathways and are considered to be closely related to the occurrence and development of DKD. This article explained some pathways and the role of podocyte autophagy and ERS in DKD, and the interaction between podocyte autophagy and ERS, which providing some potential targets for the treatment of DKD by interfering with podocyte autophagy and ERS.

摘要

糖尿病肾病(DKD)是糖尿病的严重并发症之一,已成为我国慢性肾衰竭的主要原因。足细胞是高度分化的上皮细胞,是肾小球滤过屏障的重要组成部分。足细胞的凋亡和脱落、足突融合以及裂孔膜蛋白表达降低可导致蛋白尿,进而影响DKD的进展。自噬是真核细胞降解细胞质蛋白和细胞器的重要过程,自噬水平的升高有助于减轻足细胞损伤。内质网应激(ERS)是细胞内错误折叠蛋白的积累。它使细胞进入应激状态,并且可能在两个方向上调节细胞损伤。自噬和ERS受多种信号通路调节,被认为与DKD的发生发展密切相关。本文阐述了足细胞自噬和ERS在DKD中的一些途径和作用,以及足细胞自噬与ERS之间的相互作用,为通过干扰足细胞自噬和ERS治疗DKD提供了一些潜在靶点。

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