Department of Physiology, Michigan State University, East Lansing, MI 48824, United States.
Int J Biochem Cell Biol. 2012 Mar;44(3):465-8. doi: 10.1016/j.biocel.2011.11.019. Epub 2011 Nov 30.
A large body of evidence demonstrates that angiotensin II and angiotensin receptors are required for the pathogenesis of experimental lung fibrosis. Angiotensin has a number of profibrotic effects on lung parenchymal cells that include the induction of growth factors for mesenchymal cells, extracellular matrix molecules, cytokines and increased motility of lung fibroblasts. Angiotensin is also proapoptotic for lung epithelial cells, and is synthesized by a local system (i.e., entirely within the lung tissue) after lung injury by a variety of agents of both xenobiotic and endogenous origins. Recent evidence shows that the counterregulatory molecule angiotensin 1-7, the product of the enzyme ACE-2, inhibits epithelial cell apoptosis and thus acts as an antifibrotic epithelial survival factor. This manuscript reviews the evidence supporting a role for angiotensin in lung fibrogenesis and discusses the signalling mechanisms underlying its action on lung parenchymal cells important in the pathogenesis of pulmonary fibrosis.
大量证据表明，血管紧张素 II 和血管紧张素受体是实验性肺纤维化发病机制所必需的。血管紧张素有许多致肺实质细胞纤维化的作用，包括诱导间充质细胞的生长因子、细胞外基质分子、细胞因子和增加肺成纤维细胞的迁移性。血管紧张素也促进肺上皮细胞凋亡，并且在肺损伤后由多种外源性和内源性来源的物质通过局部系统（即在肺组织内完全）合成。最近的证据表明，拮抗分子血管紧张素 1-7，即酶 ACE-2 的产物，抑制上皮细胞凋亡，因此作为上皮细胞存活的抗纤维化因子发挥作用。本文综述了血管紧张素在肺纤维化发病机制中的作用的证据，并讨论了其在肺实质细胞中的作用的信号机制，这对肺纤维化的发病机制很重要。
