Cardioprotection by Vanadium Compounds Targeting Akt-Mediated Signaling

Journal of Pharmacological Sciences

Md. Shenuarin Bhuiyan¹  Kohji Fukunaga¹ 

[1] Department of Pharmacology, Graduate School of Pharmaceutical Sciences, Tohoku University, Japan

关键词: myocardial hypertrophy;    myocardial ischemia/reperfusion;    bis(1-oxy-2-pyridinethiolato) oxovanadium (IV) [VO(OPT)];    protein kinase B/Akt;   

DOI  :  10.1254/jphs.09R01CR

学科分类：药学

来源: Nihon Yakuri Gakkai Henshuubu / Japanese Pharmacological Society

【 摘 要 】

References(137)Cited-By(27)Treatment with inorganic and organic compounds of vanadium has been shown to exert a wide range of cardioprotective effects in myocardial ischemia/reperfusion-induced injury, myocardial hypertrophy, hypertension, and vascular diseases. Furthermore, administration of vanadium compounds improves cardiac performance and smooth muscle cell contractility and modulates blood pressure in various models of hypertension. Like other vanadium compounds, we documented bis(1-oxy-2-pyridinethiolato) oxovanadium (IV) [VO(OPT)] as a potent cardioprotective agent to elicit cardiac functional recovery in myocardial infarction and pressure overload–induced hypertrophy. Vanadium compounds activate Akt signaling through inhibition of protein tyrosine phosphatases, thereby eliciting cardioprotection in myocardial ischemia/reperfusion-induced injury and myocardial hypertrophy. Vanadium compounds also promote cardiac functional recovery by stimulation of glucose transport in diabetic heart. We here discuss the current understanding of mechanisms underlying vanadium compound–induced cardioprotection and propose a novel therapeutic strategy targeting for Akt signaling to rescue cardiomyocytes from heart failure.

【 授权许可】

Unknown