Oxidative stress and cardiac repair/remodeling following infarction.
Extensive cardiac remodeling after myocardial infarction (MI) contributes significantly to ventricular dysfunction. Factors regulating left ventricular remodeling at different stages after MI are under investigation. There is growing recognition and experimental evidence that oxidative stress mediated by reactive oxygen species plays a role in the pathogeneses of myocardial repair/remodeling in various cardiac diseases. After acute MI, oxidative stress is developed in both infarcted and noninfarcted myocardium. Accumulating evidence has demonstrated that oxidative stress participates in several aspects of cardiac repair/remodeling after infarction that include cardiomyocyte apoptosis, inflammatory/fibrogenic responses, and hypertrophy. The exact pathways on reactive oxygen species-mediated myocardial remodeling are under investigation. The therapeutic potential of oxidative stress-directed drugs in myocardial remodeling after infarction has not been fully realized.
Sun
Yao
Y
Division of Cardiovascular Diseases, Department of Medicine, University of Tennessee, Health Science Center, Memphis, Tennessee 38163, USA. yasun@utmem.edu
D017209:Apoptosis; D005355:Fibrosis; D006801:Humans; D006878:Hydroxides / Q000378:metabolism; D007249:Inflammation; D009203:Myocardial Infarction / Q000473:pathology / Q000503:physiopathology*; D032383:Myocytes, Cardiac / Q000473:pathology* / Q000502:physiology; D018384:Oxidative Stress / Q000502:physiology*; D030421:Peroxynitrous Acid / Q000378:metabolism; D013481:Superoxides / Q000378:metabolism; D020257:Ventricular Remodeling / Q000502:physiology*
D006878:Hydroxides; D013481:Superoxides; D030421:Peroxynitrous Acid; C031356:hydroxide ion