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糖尿病肾病进展过程中足细胞病的表观遗传学和内质网。

Epigenetics and endoplasmic reticulum in podocytopathy during diabetic nephropathy progression.

机构信息

Department of Pharmacy, Shenzhen Longhua District Central Hospital, The Affiliated Central Hospital of Shenzhen Longhua District, Guangdong Medical University, Shenzhen, China.

Department of Pharmacy, Shenzhen Hospital, Southern Medical University, Shenzhen, China.

出版信息

Front Immunol. 2022 Dec 22;13:1090989. doi: 10.3389/fimmu.2022.1090989. eCollection 2022.

Abstract

Proteinuria or nephrotic syndrome are symptoms of podocytopathies, kidney diseases caused by direct or indirect podocyte damage. Human health worldwide is threatened by diabetic nephropathy (DN), the leading cause of end-stage renal disease (ESRD) in the world. DN development and progression are largely dependent on inflammation. The effects of podocyte damage on metabolic disease and inflammatory disorders have been documented. Epigenetic and endoplasmic reticulum (ER) stress are also evident in DN. Targeting inflammation pathway and ER stress in podocytes may be a prospective therapy to prevent the progression of DN. Here, we review the mechanism of epigenetics and ER stress on podocyte inflammation and apoptosis, and discuss the potential amelioration of podocytopathies by regulating epigenetics and ER stress as well as by targeting inflammatory signaling, which provides a theoretical basis for drug development to ameliorate DN.

摘要

蛋白尿或肾病综合征是足细胞病的症状,是由足细胞直接或间接损伤引起的肾脏疾病。糖尿病肾病(DN)是世界范围内威胁人类健康的疾病,是世界上导致终末期肾病(ESRD)的主要原因。DN 的发生和进展在很大程度上依赖于炎症。已经有文献证明足细胞损伤对代谢疾病和炎症紊乱的影响。DN 中也存在表观遗传和内质网(ER)应激。针对足细胞炎症途径和 ER 应激可能是预防 DN 进展的一种有前景的治疗方法。在这里,我们综述了表观遗传和 ER 应激对足细胞炎症和凋亡的作用机制,并讨论了通过调节表观遗传和 ER 应激以及靶向炎症信号来改善足细胞病的潜在方法,为改善 DN 的药物开发提供了理论基础。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e3e/9813850/553369bfb27d/fimmu-13-1090989-g001.jpg

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