Soon Russell K, Yee Hal F
Department of Medicine and Liver Center, University of California, San Francisco, CA 94110, USA.
Clin Liver Dis. 2008 Nov;12(4):791-803, viii. doi: 10.1016/j.cld.2008.07.004.
The contraction of hepatic stellate cells has been proposed to mediate fibrosis by regulating sinusoidal blood flow and extracellular matrix remodeling. Abundant data from diverse, yet complementary, experimental methods support a robust model for the regulation of contractile force generation by stellate cells. In this model, soluble factors associated with liver injury, including endothelin 1 and nitric oxide, are transduced primarily through Rho signaling pathways that promote the myosin II-powered generation of contractile force by stellate cells. The enhanced knowledge of the role and differential regulation of stellate cell contraction may facilitate the discovery of new and targeted strategies for the prevention and treatment of hepatic fibrosis.
肝星状细胞的收缩被认为可通过调节肝血窦血流和细胞外基质重塑来介导纤维化。来自多种互补实验方法的大量数据支持了一个关于星状细胞收缩力产生调节的强大模型。在这个模型中，与肝损伤相关的可溶性因子，包括内皮素1和一氧化氮，主要通过Rho信号通路进行转导，该信号通路促进星状细胞以肌球蛋白II为动力产生收缩力。对星状细胞收缩作用及其差异调节的深入了解可能有助于发现预防和治疗肝纤维化的新的靶向策略。
