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Target Concepts:
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Query: UMLS:C0151744 (
myocardial ischemia
)
31,282
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
VO(
OPT
), bis(1-oxy-2-pyridinethiolato)oxovanadium(IV), has been shown to increase tyrosine phosphorylation of proteins and promote the insulin receptor signaling, thereby elicit anti-diabetic action. We here investigated the cytoprotective action of VO(
OPT
) on myocardial infarction and cardiac functional recovery in rats subjected to
myocardial ischemia
/reperfusion and defined mechanisms underlying its cytoprotective action. Rats underwent 30 min
myocardial ischemia
by left anterior descending coronary artery occlusion followed by 24 h reperfusion. Post-ischemic treatment with VO(
OPT
) significantly reduced infarct size and improved cardiac function (left ventricular developed pressure and +/-dP/dt) after 72 h reperfusion and in a dose-dependent manner. Moreover, VO(
OPT
) treatment also dose-dependently significantly inhibited caspases-3, -9 and -7 processing, thereby elicited the anti-apoptotic effect. The cytoprotective effect of VO(
OPT
) was closely associated with restoration of Akt activity. The recovered Akt activity correlated with increased phosphorylation of Bad and forkhead transcription proteins, thereby inhibiting apoptotic signaling. Furthermore, treatment with VO(
OPT
) significantly increased FLIP expression, and decreased expression of Fas ligand and Bim in cardiomyocytes. Taken together, cardiomyocytes rescue following post-treatment with VO(
OPT
) from ischemia/reperfusion injury was mediated by increased FLIP expression and decreased Fas ligand and Bim expression via activation of Akt. These results demonstrate that treatment with VO(
OPT
) exerts significant cytoprotective effects along with improvement of cardiac functional recovery.
...
PMID:Cytoprotective effect of bis(1-oxy-2-pyridinethiolato)oxovanadiun(IV) on myocardial ischemia/reperfusion injury elicits inhibition of Fas ligand and Bim expression and elevation of FLIP expression. 1765 9
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.
...
PMID:Cardioprotection by vanadium compounds targeting Akt-mediated signaling. 1942 51
