Purnomo Yudi, Piccart Yvette, Coenen Tamara, Prihadi John S, Lijnen Paul J
Hypertension Unit, Campus Gasthuisberg, Herestraat 49 Box 702, B-3000 Leuven, Belgium.
Cardiovasc Hematol Disord Drug Targets. 2013 Aug;13(2):165-72. doi: 10.2174/1871529x11313020010.
A chronic increase in reactive oxygen species (ROS) plays a critical role in the development and progression of cardiac remodeling associated with heart failure. Oxidative stress is indeed increased in heart failure, hypertension, cardiac fibrosis and hypertrophy. In vitro exposure of cardiac fibroblasts to superoxide anion stimulates their proliferation by increasing the production of transforming growth factor-β1 (TGF-β1), a potent fibrogenic cytokine. TGF-β1 plays an important role in cardiac development, cardiac hypertrophy, ventricular remodeling and the early response to myocardial infarction. In this review the role of TGF-β1 and ROS in the production and deposition of collagens by cardiac fibroblasts and in the induction of gene expression in relation to the development of myocardial fibrosis and to myocardial tissue repair will be discussed.
活性氧（ROS）的长期增加在与心力衰竭相关的心脏重塑的发生和发展中起关键作用。事实上，在心力衰竭、高血压、心脏纤维化和肥大过程中氧化应激会增加。体外将心脏成纤维细胞暴露于超氧阴离子可通过增加转化生长因子-β1（TGF-β1，一种强效的促纤维化细胞因子）的产生来刺激其增殖。TGF-β1在心脏发育、心脏肥大、心室重塑以及心肌梗死的早期反应中起重要作用。在本综述中，将讨论TGF-β1和ROS在心脏成纤维细胞产生和沉积胶原蛋白以及与心肌纤维化发展和心肌组织修复相关的基因表达诱导中的作用。
