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肝纤维化中的自噬

Autophagy in hepatic fibrosis.

作者信息

Song Yang, Zhao Yingying, Wang Fei, Tao Lichan, Xiao Junjie, Yang Changqing

机构信息

Division of Gastroenterology and Hepatology, Digestive Disease Institute, Shanghai Tongji Hospital, Tongji University School of Medicine, 389 Xincun Road, Shanghai 200065, China.

Regeneration Lab and Experimental Center of Life Sciences, School of Life Science, Shanghai University, 333 Nan Chen Road, Shanghai 200444, China ; Department of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.

出版信息

Biomed Res Int. 2014;2014:436242. doi: 10.1155/2014/436242. Epub 2014 Mar 23.

DOI:10.1155/2014/436242
PMID:24779010
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3980865/
Abstract

Hepatic fibrosis is a leading cause of morbidity and mortality worldwide. Hepatic fibrosis is usually associated with chronic liver diseases caused by infection, drugs, metabolic disorders, or autoimmune imbalances. Effective clinical therapies are still lacking. Autophagy is a cellular process that degrades damaged organelles or protein aggregation, which participates in many pathological processes including liver diseases. Autophagy participates in hepatic fibrosis by activating hepatic stellate cells and may participate as well through influencing other fibrogenic cells. Besides that, autophagy can induce some liver diseases to develop while it may play a protective role in hepatocellular abnormal aggregates related liver diseases and reduces fibrosis. With a better understanding of the potential effects of autophagy on hepatic fibrosis, targeting autophagy might be a novel therapeutic strategy for hepatic fibrosis in the near future.

摘要

肝纤维化是全球发病和死亡的主要原因。肝纤维化通常与由感染、药物、代谢紊乱或自身免疫失衡引起的慢性肝病相关。目前仍缺乏有效的临床治疗方法。自噬是一种降解受损细胞器或蛋白质聚集体的细胞过程,它参与包括肝脏疾病在内的许多病理过程。自噬通过激活肝星状细胞参与肝纤维化,也可能通过影响其他致纤维化细胞发挥作用。除此之外,自噬可诱导一些肝脏疾病的发生,而在与肝细胞异常聚集相关的肝脏疾病中可能发挥保护作用并减轻纤维化。随着对自噬对肝纤维化潜在影响的更深入了解,靶向自噬可能在不久的将来成为肝纤维化的一种新型治疗策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d2b3/3980865/7f220cde7d72/BMRI2014-436242.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d2b3/3980865/7f220cde7d72/BMRI2014-436242.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d2b3/3980865/7f220cde7d72/BMRI2014-436242.001.jpg

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