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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Format: | Article |
Language: | English |
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Elsevier
2009-01-01
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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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format | Article |
id | doaj.art-085c2c67ef90469398cf69fba220a1ec |
institution | Directory Open Access Journal |
issn | 1347-8613 |
language | English |
last_indexed | 2024-12-23T20:40:49Z |
publishDate | 2009-01-01 |
publisher | Elsevier |
record_format | Article |
series | Journal of Pharmacological Sciences |
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 |
work_keys_str_mv | AT mdshenuarinbhuiyan cardioprotectionbyvanadiumcompoundstargetingaktmediatedsignaling AT kohjifukunaga cardioprotectionbyvanadiumcompoundstargetingaktmediatedsignaling |