Cardioprotection by Vanadium Compounds Targeting Akt-Mediated Signaling

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 imp...

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Main Authors: Md. Shenuarin Bhuiyan, Kohji Fukunaga
Format: Article
Language:English
Published: Elsevier 2009-01-01
Series:Journal of Pharmacological Sciences
Online Access:http://www.sciencedirect.com/science/article/pii/S1347861319312083
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author Md. Shenuarin Bhuiyan
Kohji Fukunaga
author_facet Md. Shenuarin Bhuiyan
Kohji Fukunaga
author_sort Md. Shenuarin Bhuiyan
collection DOAJ
description 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. Keywords:: myocardial hypertrophy, myocardial ischemia/reperfusion, bis(1-oxy-2-pyridinethiolato) oxovanadium (IV) [VO(OPT)], protein kinase B/Akt
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spelling doaj.art-085c2c67ef90469398cf69fba220a1ec2022-12-21T17:31:56ZengElsevierJournal of Pharmacological Sciences1347-86132009-01-011101113Cardioprotection by Vanadium Compounds Targeting Akt-Mediated SignalingMd. Shenuarin Bhuiyan0Kohji Fukunaga1Department of Pharmacology, Graduate School of Pharmaceutical Sciences, Tohoku University, Aramaki-Aoba, Aoba-ku, Sendai 980-8578, JapanDepartment of Pharmacology, Graduate School of Pharmaceutical Sciences, Tohoku University, Aramaki-Aoba, Aoba-ku, Sendai 980-8578, Japan; Tohoku University 21st Century COE Program “CRESCENDO”, Sendai 980-8578, Japan; Corresponding author. fukunaga@mail.pharm.tohoku.ac.jpAbstract.: 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. Keywords:: myocardial hypertrophy, myocardial ischemia/reperfusion, bis(1-oxy-2-pyridinethiolato) oxovanadium (IV) [VO(OPT)], protein kinase B/Akthttp://www.sciencedirect.com/science/article/pii/S1347861319312083
spellingShingle Md. Shenuarin Bhuiyan
Kohji Fukunaga
Cardioprotection by Vanadium Compounds Targeting Akt-Mediated Signaling
Journal of Pharmacological Sciences
title Cardioprotection by Vanadium Compounds Targeting Akt-Mediated Signaling
title_full Cardioprotection by Vanadium Compounds Targeting Akt-Mediated Signaling
title_fullStr Cardioprotection by Vanadium Compounds Targeting Akt-Mediated Signaling
title_full_unstemmed Cardioprotection by Vanadium Compounds Targeting Akt-Mediated Signaling
title_short Cardioprotection by Vanadium Compounds Targeting Akt-Mediated Signaling
title_sort cardioprotection by vanadium compounds targeting akt mediated signaling
url http://www.sciencedirect.com/science/article/pii/S1347861319312083
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AT kohjifukunaga cardioprotectionbyvanadiumcompoundstargetingaktmediatedsignaling