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Cardioprotection by vanadium compounds targeting Akt-mediated signaling
M Shenuarin Bhuiyan1, Kohji Fukunaga
1Department of Pharmacology, Tohoku University, Japan.
Abstract:
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.
Insights
Vanadium compounds, including bis(1-oxy-2-pyridinethiolato) oxovanadium (IV) [VO(OPT)], offer significant cardioprotection against heart diseases. They activate Akt signaling, improving cardiac function and potentially rescuing cardiomyocytes from heart failure.
Area of Science:
- Cardiovascular Pharmacology
- Medicinal Chemistry
- Biochemistry
Background:
- Vanadium compounds exhibit diverse cardioprotective effects in conditions like myocardial ischemia/reperfusion, hypertrophy, and hypertension.
- These compounds improve cardiac performance, smooth muscle contractility, and blood pressure regulation.
- Bis(1-oxy-2-pyridinethiolato) oxovanadium (IV) [VO(OPT)] is identified as a potent agent for cardiac functional recovery.
Purpose of the Study:
- To elucidate the mechanisms underlying vanadium compound-induced cardioprotection.
- To investigate the role of Akt signaling in vanadium-mediated cardiac protection.
- To propose a therapeutic strategy for heart failure targeting Akt signaling.
Main Methods:
- Review of existing literature on vanadium compounds and their cardiovascular effects.
- Analysis of signaling pathways, including Akt activation and protein tyrosine phosphatase inhibition.
- Discussion of therapeutic potential in models of myocardial infarction, hypertrophy, and diabetic heart disease.
Main Results:
- Vanadium compounds activate Akt signaling by inhibiting protein tyrosine phosphatases.
- This activation leads to cardioprotection in myocardial ischemia/reperfusion and hypertrophy.
- Vanadium compounds enhance glucose transport in diabetic hearts, promoting functional recovery.
Conclusions:
- Vanadium compounds, particularly [VO(OPT)], demonstrate significant cardioprotective properties.
- Targeting Akt signaling represents a promising therapeutic strategy for heart failure.
- Further research into vanadium-based therapies could offer novel treatments for cardiovascular diseases.
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