Parola Maurizio, Marra Fabio, Pinzani Massimo
Dipartimento di Medicina e Oncologia Sperimentale, University of Torino, Corso Raffaello 30, 10125 Torino, Italy.
Mol Aspects Med. 2008 Feb-Apr;29(1-2):58-66. doi: 10.1016/j.mam.2007.09.002. Epub 2007 Oct 7.
Fibrotic progression of chronic liver diseases of different aetiology to the common advanced-stage of cirrhosis can be envisaged as a dynamic and highly integrated cellular response to chronic liver injury. Liver fibrosis is accompanied by perpetuation of liver injury, chronic hepatitis and persisting activation of tissue repair mechanisms, leading eventually to excess deposition of ECM components. Liver fibrogenesis (i.e., the process) is sustained by populations of highly proliferative, pro-fibrogenic and contractile MFs that, according to current literature, originate by a process of activation involving perisinusoidal HSC, portal fibroblasts and even bone marrow-derived MSC. In this short review emerging concepts in hepatic fibrogenesis and related molecular mechanisms, as provided by recent experimental and clinical studies, are presented.
不同病因的慢性肝病向常见的晚期肝硬化的纤维化进展可被设想为对慢性肝损伤的一种动态且高度整合的细胞反应。肝纤维化伴随着肝损伤的持续、慢性肝炎以及组织修复机制的持续激活，最终导致细胞外基质（ECM）成分过度沉积。肝纤维化形成（即这个过程）由高度增殖、促纤维化且具有收缩性的肌成纤维细胞（MFs）群体维持，根据当前文献，这些细胞起源于一个涉及窦周肝星状细胞（HSC）、门静脉成纤维细胞甚至骨髓来源的间充质干细胞（MSC）的激活过程。在这篇简短的综述中，将介绍近期实验和临床研究提供的肝纤维化形成中的新观念及相关分子机制。
