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足细胞自噬:预防糖尿病肾病进展的潜在治疗靶点。

Podocyte Autophagy: A Potential Therapeutic Target to Prevent the Progression of Diabetic Nephropathy.

作者信息

Liu Na, Xu Liuqing, Shi Yingfeng, Zhuang Shougang

机构信息

Department of Nephrology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.

Department of Medicine, Rhode Island Hospital and Alpert Medical School, Brown University, Providence, RI, USA.

出版信息

J Diabetes Res. 2017;2017:3560238. doi: 10.1155/2017/3560238. Epub 2017 Apr 23.

Abstract

Diabetic nephropathy (DN), a leading cause of end-stage renal disease (ESRD), becomes a worldwide problem. Ultrastructural changes of the glomerular filtration barrier, especially the pathological changes of podocytes, lead to proteinuria in patients with diabetes. Podocytes are major components of glomerular filtration barrier, lining outside of the glomerular basement membrane (GBM) to maintain the permeability of the GBM. Autophagy is a high conserved cellular process in lysosomes including impaired protein, cell organelles, and other contents in the cytoplasm. Recent studies suggest that activation of autophagy in podocytes may be a potential therapy to prevent the progression of DN. Here, we review the mechanisms of autophagy in podocytes and discuss the current studies about alleviating proteinuria via activating podocyte autophagy.

摘要

糖尿病肾病(DN)是终末期肾病(ESRD)的主要病因,已成为一个全球性问题。肾小球滤过屏障的超微结构变化,尤其是足细胞的病理变化,导致糖尿病患者出现蛋白尿。足细胞是肾小球滤过屏障的主要组成部分,排列在肾小球基底膜(GBM)外侧以维持GBM的通透性。自噬是一种在溶酶体中高度保守的细胞过程,包括受损蛋白质、细胞器和细胞质中的其他成分。最近的研究表明,激活足细胞中的自噬可能是预防DN进展的一种潜在治疗方法。在此,我们综述足细胞自噬的机制,并讨论目前关于通过激活足细胞自噬减轻蛋白尿的研究。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98e0/5420432/530123f2c018/JDR2017-3560238.001.jpg

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