Suppr超能文献

自噬在衰老和慢性胆汁淤积性疾病中的作用。

Involvement of Autophagy in Ageing and Chronic Cholestatic Diseases.

机构信息

Department of Gastroenterology and Hepatology, Università Politecnica delle Marche, 60126 Ancona, Italy.

出版信息

Cells. 2021 Oct 16;10(10):2772. doi: 10.3390/cells10102772.

Abstract

Autophagy is a "housekeeping" lysosomal degradation process involved in numerous physiological and pathological processes in all eukaryotic cells. The dysregulation of hepatic autophagy has been described in several conditions, from obesity to diabetes and cholestatic disease. We review the role of autophagy, focusing on age-related cholestatic diseases, and discuss its therapeutic potential and the molecular targets identified to date. The accumulation of toxic BAs is the main cause of cell damage in cholestasis patients. BAs and their receptor, FXR, have been implicated in the regulation of hepatic autophagy. The mechanisms by which cholestasis induces liver damage include mitochondrial dysfunction, oxidative stress and ER stress, which lead to cell death and ultimately to liver fibrosis as a compensatory mechanism to reduce the damage. The stimulation of autophagy seems to ameliorate the liver damage. Autophagic activity decreases with age in several species, whereas its basic extends lifespan in animals, suggesting that it is one of the convergent mechanisms of several longevity pathways. No strategies aimed at inducing autophagy have yet been tested in cholestasis patients. However, its stimulation can be viewed as a novel therapeutic strategy that may reduce ageing-dependent liver deterioration and also mitigate hepatic steatosis.

摘要

自噬是一种“管家”溶酶体降解过程,参与所有真核细胞中的许多生理和病理过程。肝自噬的失调已在多种情况下被描述,从肥胖到糖尿病和胆汁淤积性疾病。我们回顾了自噬的作用,重点关注与年龄相关的胆汁淤积性疾病,并讨论了其治疗潜力和迄今为止确定的分子靶点。有毒 BAs 的积累是胆汁淤积症患者细胞损伤的主要原因。BAs 和它们的受体 FXR 被认为参与了肝自噬的调节。胆汁淤积症引起肝损伤的机制包括线粒体功能障碍、氧化应激和 ER 应激,这些机制导致细胞死亡,最终导致肝纤维化作为减少损伤的代偿机制。自噬的刺激似乎可以改善肝损伤。在几种物种中,自噬活性随着年龄的增长而下降,而其基本功能在动物中延长了寿命,这表明它是几种长寿途径的收敛机制之一。目前还没有针对胆汁淤积症患者的诱导自噬的策略。然而,刺激自噬可以被视为一种新的治疗策略,可能减少与年龄相关的肝恶化,并减轻肝脂肪变性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd49/8534511/d824e999ff20/cells-10-02772-g001.jpg

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验