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自噬和 NLRP3 炎性小体在肝纤维化中的作用。

The Role of Autophagy and NLRP3 Inflammasome in Liver Fibrosis.

机构信息

Occupational and Environmental Health Department, Dalian Medical University, 9 Lvshun South Road, Dalian 116044, China.

Nutrition and Food Hygiene, Dalian Medical University, 9 Lvshun South Road, Dalian 116044, China.

出版信息

Biomed Res Int. 2020 Jul 11;2020:7269150. doi: 10.1155/2020/7269150. eCollection 2020.

Abstract

Liver fibrosis is an intrinsic repair process of chronic injury with excessive deposition of extracellular matrix. As an early stage of various liver diseases, liver fibrosis is a reversible pathological process. Therefore, if not being controlled in time, liver fibrosis will evolve into cirrhosis, liver failure, and liver cancer. It has been demonstrated that hepatic stellate cells (HSCs) play a crucial role in the formation of liver fibrosis. In particular, the activation of HSCs is a key step for liver fibrosis. Recent researches have suggested that autophagy and inflammasome have biological effect on HSC activation. Herein, we review current studies about the impact of autophagy and NOD-like receptors containing pyrin domain 3 (NLRP3) inflammasome on liver fibrosis and the underlying mechanisms.

摘要

肝纤维化是慢性损伤时细胞外基质过度沉积的固有修复过程。作为各种肝病的早期阶段,肝纤维化是一种可逆转的病理过程。因此,如果不能及时得到控制,肝纤维化将发展为肝硬化、肝衰竭和肝癌。已经证明肝星状细胞(HSCs)在肝纤维化的形成中起着关键作用。特别是,HSCs 的激活是肝纤维化的关键步骤。最近的研究表明,自噬和包含 NOD 样受体含pyrin 域 3(NLRP3)的炎性小体对 HSC 激活具有生物学作用。本文综述了自噬和 NLRP3 炎性小体对肝纤维化的影响及其潜在机制的研究进展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf2d/7369671/f391eb01db8e/BMRI2020-7269150.001.jpg

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