Valfrè di Bonzo Lorenzo, Novo Erica, Cannito Stefania, Busletta Chiara, Paternostro Claudia, Povero Davide, Parola Maurizio
Department of Experimental Medicine and Oncology and Interuniversitary Centre of Hepatic Pathophysiology, University of Torino, Italy.
Histol Histopathol. 2009 Oct;24(10):1323-41. doi: 10.14670/HH-24.1323.
Angiogenesis is a dynamic, hypoxia-stimulated and growth factor-dependent process, eventually leading to the formation of new vessels from pre-existing blood vessels. In the last decade experimental and clinical studies have described the occurrence of hepatic angiogenesis in a number of different pathophysiological conditions, including those involving inflammatory, fibrotic and ischemic features. In particular, the literature evidence indicates that hepatic angiogenesis is strictly associated with, and may even favour fibrogenic progression of chronic inflammatory liver diseases of different aetiology. In this review, current "in vivo" and "in vitro" evidence supporting the potential pathogenetic role of angiogenesis in chronic liver diseases will be reviewed in an attempt to outline cellular and molecular mechanisms involved, with a specific emphasis on the crucial role of hypoxic conditions and hepatic stellate cells (HSCs), particularly when activated to the myofibroblast-like pro-fibrogenic phenotype.
血管生成是一个动态的、由缺氧刺激且依赖生长因子的过程，最终导致从已有的血管形成新的血管。在过去十年中，实验和临床研究描述了在许多不同的病理生理状况下肝脏血管生成的发生情况，包括那些具有炎症、纤维化和缺血特征的状况。特别是，文献证据表明肝脏血管生成与不同病因的慢性炎症性肝病的纤维化进展密切相关，甚至可能促进其纤维化进展。在本综述中，将回顾支持血管生成在慢性肝病中潜在致病作用的当前“体内”和“体外”证据，试图概述其中涉及的细胞和分子机制，特别强调缺氧条件和肝星状细胞（HSCs）的关键作用，尤其是当它们被激活为肌成纤维细胞样促纤维化表型时。
