Atamas Sergei P
Division of Rheumatology and Clinical Immunology, Department of Medicine, University of Maryland School of Medicine, MSTF building, Room 8-34, 10 South Pine Street, Baltimore 21201, USA.
Life Sci. 2002 Dec 27;72(6):631-43. doi: 10.1016/s0024-3205(02)02299-3.
Tissue fibrosis, a serious and even deadly complication of chronic inflammation and environmental exposures, is regulated by a host of factors including interactions with the extracellular matrix, surface of inflammatory cells, hormones, and an extremely complex and redundant network of profibrotic cytokines. The nature of mechanisms by which cytokines regulate fibrosis is dual - indirect, through attraction of inflammatory cells, and direct, through binding to specific receptors on fibroblasts and stimulating proliferation, collagen production and secretion of autocrine factors. This review focuses on systematizing the direct effects of cytokines on fibroblasts. Understanding of the complexity of the cytokine-driven mechanisms of fibrosis is important for identification of potential molecular targets for future pharmacological interventions in prevention and treatment of tissue fibrosis.
组织纤维化是慢性炎症和环境暴露的一种严重甚至致命的并发症，它受许多因素调控，包括与细胞外基质、炎症细胞表面、激素以及极其复杂且冗余的促纤维化细胞因子网络的相互作用。细胞因子调节纤维化的机制具有双重性——间接作用是通过吸引炎症细胞，直接作用是通过与成纤维细胞上的特定受体结合并刺激其增殖、胶原蛋白产生以及自分泌因子的分泌。本综述着重于系统梳理细胞因子对成纤维细胞的直接作用。了解细胞因子驱动的纤维化机制的复杂性，对于确定未来预防和治疗组织纤维化的药物干预潜在分子靶点具有重要意义。
