Moreno Montserrat, Bataller Ramon
Liver Unit, Institut Clínic de Malalties Digestives i Metabòliques, Hospital Clínic, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Catalonia, Spain.
Clin Liver Dis. 2008 Nov;12(4):825-52, ix. doi: 10.1016/j.cld.2008.07.013.
Hepatic fibrosis is the result of a complex interplay between resident hepatic cells, infiltrating inflammatory cells, and a number of locally acting peptides called cytokines. Key mediators include transforming growth factor b1, vasoactive substances, adipokines, inflammatory cytokines and chemokines. Angiotensin II, the main effector of the renin-angiotensin system, is a true cytokine that plays a major role in liver fibrosis. Angiotensin II is locally synthesized in the injured liver and induces profibrogenic actions in hepatic stellate cells. Drugs blocking the renin-angiotensin system are promising antifibrotic agents. There are multiple signal transduction pathways involved in cytokine signaling. Drugs interfering intracellular pathways involved in increased collagen production are potential therapies for liver fibrosis.
肝纤维化是驻留肝细胞、浸润性炎症细胞以及一些被称为细胞因子的局部作用肽之间复杂相互作用的结果。关键介质包括转化生长因子β1、血管活性物质、脂肪因子、炎性细胞因子和趋化因子。肾素-血管紧张素系统的主要效应物血管紧张素II是一种真正的细胞因子,在肝纤维化中起主要作用。血管紧张素II在受损肝脏中局部合成,并在肝星状细胞中诱导促纤维化作用。阻断肾素-血管紧张素系统的药物是有前景的抗纤维化药物。细胞因子信号传导涉及多个信号转导途径。干扰参与胶原生成增加的细胞内途径的药物是肝纤维化的潜在治疗方法。