Ihn Hironobu
Department of Dermatology, Faculty of Medicine, University of Tokyo, Japan.
Curr Opin Rheumatol. 2002 Nov;14(6):681-5. doi: 10.1097/00002281-200211000-00009.
Transforming growth factor (TGF)-beta regulates diverse biologic activities including cell growth, cell death or apoptosis, cell differentiation, and extracellular matrix (ECM) synthesis. TGF-beta is believed to be a key mediator of tissue fibrosis as a consequence of ECM accumulation in pathologic states such as systemic sclerosis. TGF-beta is known to induce the expression of ECM proteins in mesenchymal cells, and to stimulate the production of protease inhibitors that prevent enzymatic breakdown of the ECM. Connective tissue growth factor (CTGF), which is induced by TGF-beta, has been reported to mediate stimulatory actions of TGF-beta ECM synthesis. This review focuses on the possible role of TGF-beta and CTGF in the pathogenesis of fibrosis.
转化生长因子（TGF）-β调节多种生物学活性，包括细胞生长、细胞死亡或凋亡、细胞分化以及细胞外基质（ECM）合成。由于在系统性硬化症等病理状态下ECM积累，TGF-β被认为是组织纤维化的关键介质。已知TGF-β可诱导间充质细胞中ECM蛋白的表达，并刺激蛋白酶抑制剂的产生，从而防止ECM的酶解。据报道，由TGF-β诱导的结缔组织生长因子（CTGF）介导TGF-β对ECM合成的刺激作用。本综述重点关注TGF-β和CTGF在纤维化发病机制中的可能作用。
