Holt Andrew P, Salmon Mike, Buckley Christopher D, Adams David H
Liver Research Group, MRC Centre for Immune Regulation, University of Birmingham, Birmingham, UK.
Clin Liver Dis. 2008 Nov;12(4):861-82, x. doi: 10.1016/j.cld.2008.07.002.
Liver cirrhosis is caused by iterative cycles of tissue injury, inflammation, and repair. Although most causes of acute hepatitis resolve without scarring, chronic hepatitis is associated with persistent inflammation and matrix remodeling, which leads to fibrosis and, eventually, cirrhosis. The mechanisms that govern wound healing involve interactions between the innate and adaptive immune systems and stromal cells within a microenvironment composed of cytokines, growth factors, and modified matricellular proteins. The immune system plays a central role in the regulation of fibrosis, tissue repair, and recovery that is vital for the maintenance of tissue homeostasis. Chronic inflammation and fibrosis are inextricably linked and the cellular interactions between immune effector cells, local fibroblasts, and tissue macrophages at sites of scar formation determine the outcome of liver injury and the development of scarring.
肝硬化是由组织损伤、炎症和修复的反复循环引起的。虽然大多数急性肝炎的病因可在无瘢痕形成的情况下得到解决，但慢性肝炎与持续炎症和基质重塑有关，这会导致纤维化，并最终发展为肝硬化。伤口愈合的机制涉及先天免疫系统和适应性免疫系统与由细胞因子、生长因子和修饰的基质细胞蛋白组成的微环境中的基质细胞之间的相互作用。免疫系统在纤维化、组织修复和恢复的调节中起着核心作用，这对于维持组织内环境稳定至关重要。慢性炎症和纤维化紧密相连，瘢痕形成部位的免疫效应细胞、局部成纤维细胞和组织巨噬细胞之间的细胞相互作用决定了肝损伤的结果和瘢痕形成的发展。
