Nonmetabolic effects of trimetazidine and ventricular remodeling: role in regulatory gene expression
نویسنده
چکیده
Although the management of ischemic heart disease and chronic heart failure (CHF) has made considerable progress over the past years, CHF is still a tremendous medical burden. The metabolic and therapeutic approach might play a significant role in reducing disease progression and mortality rate. The metabolic modulator trimetazidine, a partial inhibitor of long chain 3-ketoacyl CoA thiolase activity, the last enzyme involved in b-oxidation, seems to exert positive effects in the management of left ventricle remodeling in heart failure patients by reducing the progression of disease, and by improving quality of life and prognosis. Recent reports suggest that trimetazidine could also exert nonmetabolic effects useful in preventing left ventricle remodeling by modulating the expression of various regulatory genes (nitric oxide synthase, endothelin-1, tumor necrosis factors, atrial natriuretic peptide, glucose transporters) involved in endothelial and mitochondrial function, myocardial cell death, and tissue fibrosis. L Heart Metab. 2014;65:26-30
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