Regulation of Cardiac Remodeling by Nitric Oxide: Focus on Cardiac Myocyte Hypertrophy and Apoptosis

摘要: Cardiac hypertrophy occurs in pathological conditions associated with chronic increases hemodynamic load. Although can initially be viewed as a salutary response, ultimately, it often enters phase of remodeling that may lead to heart failure and premature death. A prevailing concept predicts changes gene expression hypertrophied cardiac myocytes myocyte loss by apoptosis contribute the transition from failure. In recent years, nitric oxide (NO) has emerged an important regulator remodeling. Specifically, NO been recognized potent antihypertrophic proapoptotic mediator cultured myocytes. Studies genetically engineered mice have extended these findings vivo situation. It appears low levels transient release endothelial synthase exert beneficial effects on process reducing hypertrophy, cavity dilation mortality. By contrast, high sustained production inducible seem maladaptive ventricular contractile function, increasing apoptosis, future, novel insights into role should allow development therapeutic strategies treat