Critical roles of NADPH oxidase and reactive oxygen species in the development of cardiac hypertrophy
NADPH oxidase (NOX) enzymes catalyze the reduction of molecular oxygen (O2) to superoxide (O2),the typical primary product of this reaction,which could be further spontaneously or superoxide dismutase(SOD)dependently catalyzed to hydrogen peroxide(H2O2),or other type of reactive oxygen species (ROS).ROS function as signaling molecules and regulators of cell function when they are generated in a compartmentalized and regulated manner.The roles of NOX in the pathogenesis of pulmonary and cardiac diseases have previously been reported,including pulmonary infectious diseases,acute lung injury,pulmonary hypertension,ischemia reperfusion,etc.Recently,the role of NOX in the development of cardiac hypertrophy was also suggested.Currently,at least 7 isoforms ofNOX (NOX 1-5 and DUOX 1-2) have been identified in human by molecular cloning.Each NOX enzyme contains at least 6 subunit proteins,including gp91phox,p22phox,p67phox,p47phox,p40phox,and Rac(l).p67phox is one of the two major cytosolic subunits ofNOX.Overexpression of a dominantnegative mutant of the p67phox (DN-p67)with a V204A point mutation completely prevented NOX—mediated ROS generation in vitro.Recently,we showed that overexpression of the above DN-p67 mutant protein in adult rat ventricular myocytes attenuated α 1adrenergic receptor—stimulated cardiac hypertrophy in vitro.
Lei Xiao
Department of Medicine & Center for Cardiovascular Research, University of Illinois at Chicago
国内会议
北京
英文
10-10
2013-04-19（万方平台首次上网日期，不代表论文的发表时间）