Cardiovascular Protection with Vanadium Compounds

Protein kinase B/Akt plays a critical role in the regulation of cardiac hypertrophy, angiogenesis and apoptosis. The evidences that elevation of Akt in cardiomyocytes in vivo and in vitro protects against apoptosis after ischemia/reperfusion injury provide possibility that agents targeting Akt activation become a novel therapeutic strategy for limiting myocardial injury following ischemia. Vanadium compounds inhibiting protein tyrosine phosphatases are potent activator of the Akt signaling pathways and elicit cardioprotection in heart ischemia/reperfusion injury along with cardiac functional recovery in rats. In addition, vanadium compounds has strong anti-hypertrophic in the pressure overload-induced hypertrophy in ovariectomized and aortic-banded rats. The elevation of Akt activity and Akt-dependent eNOS phosphorylation are central roles on vanadium compound-induced anti-hypertrophy and heart failure in the ovariectomized and aortic-banded rats. Taken together, vanadium compounds are potential therapeutics for ischemia/reperfusion-induced myocardial injury and heart failure associated with hypertension in the postmenopausal women.