缺氧(环境)
纤维化
细胞外基质
缺氧诱导因子
肌成纤维细胞
病理
医学
肝纤维化
肝星状细胞
肝纤维化
生物
免疫学
癌症研究
化学
细胞生物学
生物化学
基因
氧气
有机化学
作者
Beatrice Foglia,Erica Novo,Francesca Protopapa,Marina Maggiora,Claudia Bocca,Stefania Cannito,Maurizio Parola
出处
期刊:Cells
[MDPI AG]
日期:2021-07-13
卷期号:10 (7): 1764-1764
被引量:56
标识
DOI:10.3390/cells10071764
摘要
Liver fibrosis is a potentially reversible pathophysiological event, leading to excess deposition of extracellular matrix (ECM) components and taking place as the net result of liver fibrogenesis, a dynamic and highly integrated process occurring during chronic liver injury of any etiology. Liver fibrogenesis and fibrosis, together with chronic inflammatory response, are primarily involved in the progression of chronic liver diseases (CLD). As is well known, a major role in fibrogenesis and fibrosis is played by activated myofibroblasts (MFs), as well as by macrophages and other hepatic cell populations involved in CLD progression. In the present review, we will focus the attention on the emerging pathogenic role of hypoxia, hypoxia-inducible factors (HIFs) and related mediators in the fibrogenic progression of CLD.
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