Mitochondrial reactive oxygen species (ROS) as signaling molecules of intracellular pathways triggered by the cardiac renin-angiotensin II-aldosterone system (RAAS).
Mitochondrial reactive oxygen species (ROS) as signaling molecules of intracellular pathways triggered by the cardiac renin-angiotensin II-aldosterone system (RAAS).
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DOI：
10.3389/fphys.2013.00126
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发表时间：
2013
影响因子：
4
通讯作者：
Aiello EA
中科院分区：
文献类型：
--
作者：
De Giusti VC;Caldiz CI;Ennis IL;Pérez NG;Cingolani HE;Aiello EA
线粒体是心肌细胞产生基础活性氧的主要来源。活性氧作为信号分子介导不同的细胞内途径的作用，在过去的几年中已经获得了越来越多的生理学家的兴趣。在过去的几年里，我们一直在研究线粒体活性氧在心肌中由肾素-血管紧张素II-醛固酮系统（RAAS）触发的细胞内途径中的参与。我们已经证明，急性激活心脏RAAS诱导线粒体ATP依赖性钾通道（mitoKATP）开放，从而增加线粒体ROS的产生。这些氧化剂分子，反过来，激活膜转运蛋白，钠/氢交换器（NHE-1）和钠/碳酸氢盐协同转运蛋白（NBC）通过刺激ROS敏感的MAPK级联。这种效应器的刺激导致心脏收缩力的增加。此外，这是可行的建议，一个持续增加的生产线粒体活性氧诱导慢性心脏RAAS，因此，慢性NHE-1和NBC刺激，也将导致心脏肥大的发展。
Mitochondria represent major sources of basal reactive oxygen species (ROS) production of the cardiomyocyte. The role of ROS as signaling molecules that mediate different intracellular pathways has gained increasing interest among physiologists in the last years. In our lab, we have been studying the participation of mitochondrial ROS in the intracellular pathways triggered by the renin-angiotensin II-aldosterone system (RAAS) in the myocardium during the past few years. We have demonstrated that acute activation of cardiac RAAS induces mitochondrial ATP-dependent potassium channel (mitoKATP) opening with the consequent enhanced production of mitochondrial ROS. These oxidant molecules, in turn, activate membrane transporters, as sodium/hydrogen exchanger (NHE-1) and sodium/bicarbonate cotransporter (NBC) via the stimulation of the ROS-sensitive MAPK cascade. The stimulation of such effectors leads to an increase in cardiac contractility. In addition, it is feasible to suggest that a sustained enhanced production of mitochondrial ROS induced by chronic cardiac RAAS, and hence, chronic NHE-1 and NBC stimulation, would also result in the development of cardiac hypertrophy.
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影响因子：
4.8
作者：
Bienert, Gerd P.;Moller, Anders L. B.;Jahn, Thomas P.
通讯作者：
Jahn, Thomas P.
影响因子：
--
作者：
Cingolani, HE;Pérez, NG;de Hurtado, MCC
通讯作者：
de Hurtado, MCC
影响因子：
4.8
作者：
Costa, Alexandre D. T.;Jakob, Regina;Garlid, Keith D.
通讯作者：
Garlid, Keith D.
影响因子：
6.1
作者：
De Giusti, V. C.;Correa, M. V.;Aiello, E. A.
通讯作者：
Aiello, E. A.
影响因子：
20.1
作者：
Dai DF;Johnson SC;Villarin JJ;Chin MT;Nieves-Cintrón M;Chen T;Marcinek DJ;Dorn GW 2nd;Kang YJ;Prolla TA;Santana LF;Rabinovitch PS
通讯作者：
Rabinovitch PS