Department of Medicine, University of California, San Diego, La Jolla, CA 92093-0602, USA.
Best Pract Res Clin Gastroenterol. 2011 Apr;25(2):305-17. doi: 10.1016/j.bpg.2011.02.011.
Liver fibrosis is an outcome of many chronic diseases, and often results in cirrhosis, liver failure, and portal hypertension. Liver transplantation is the only treatment available for patients with advanced stage of fibrosis. Therefore, alternative methods are required to develop new strategies for anti-fibrotic therapy. Available treatments are designed to substitute for liver transplantation or bridge the patients, they include inhibitors of fibrogenic cytokines such as TGF-β1 and EGF, inhibitors of rennin angiotensin system, and blockers of TLR4 signalling. Development of liver fibrosis is orchestrated by many cell types. However, activated myofibroblasts remain the primary target for anti-fibrotic therapy. Hepatic stellate cells and portal fibroblasts are considered to play a major role in development of liver fibrosis. Here we discuss the origin of activated myofibroblasts and different aspects of their activation, differentiation and potential inactivation during regression of liver fibrosis.
肝纤维化是许多慢性疾病的结果，常导致肝硬化、肝功能衰竭和门静脉高压。肝移植是纤维化晚期患者唯一可用的治疗方法。因此，需要开发新的抗纤维化治疗策略。现有的治疗方法旨在替代肝移植或为患者提供过渡，其中包括 TGF-β1 和 EGF 等纤维生成细胞因子的抑制剂、肾素-血管紧张素系统抑制剂和 TLR4 信号通路阻滞剂。肝纤维化的发展由许多细胞类型协调。然而，活化的肌成纤维细胞仍然是抗纤维化治疗的主要靶点。肝星状细胞和门脉成纤维细胞被认为在肝纤维化的发展中起主要作用。在这里，我们讨论了活化的肌成纤维细胞的起源以及它们在肝纤维化消退过程中的激活、分化和潜在失活的不同方面。
