Physiological and pathological functions of NADPH oxidases during myocardial ischemia–reperfusion
作者： Shouji Matsushima , Hiroyuki Tsutsui , Junichi Sadoshima
DOI: 10.1016/J.TCM.2014.03.003
关键词: Downregulation and upregulation 、 Signal transduction 、 Isozyme 、 Heart failure 、 NADPH oxidase 、 NOX4 、 Biochemistry 、 Reactive oxygen species 、 Internal medicine 、 Endocrinology 、 Oxidative stress 、 Biology
摘要: Oxidative stress, the presence of reactive oxygen species (ROS) in excess antioxidant capacity heart induces myocardial damage, accumulation which leads to ischemic disease and failure. NADPH oxidase (Nox) 2 4 are major sources O2- H2O2 play a crucial role regulation growth death cardiomyocytes. Both Nox2 Nox4 upregulated response ischemia-reperfusion (I/R), thereby contributing ROS production consequent injury. Suppression either one them can reduce I/R injury heart. Importantly, however, minimum level by or is essential for activation HIF-1α inhibition PPARα during I/R, such that combined suppression both exacerbates Thus, excessive Noxs below physiological levels induce cardiac Here we discuss detrimental salutary functions Nox isoforms I/R.
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