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Published on: July 10, 2019
Targeting protein kinase B/Akt signaling with vanadium compounds for cardioprotection
Md Shenuarin Bhuiyan1, Norifumi Shioda, Kohji Fukunaga
1Graduate School of Pharmaceutical Sciences, Department of Pharmacology, Tohoku University, Aramaki-Aoba Aoba-ku, Sendai 980-8578, Japan.
Background:
Akt is an important signaling molecule that modulates many cellular processes such as cell growth, survival and metabolism. Akt activation has been proposed as a potential strategy for increasing cardiomyocyte survival following ischemia.
Objectives:
Vanadium compounds activate Akt signaling through inhibition of protein tyrosine phosphatases, thereby eliciting cardioprotection in myocardial ischemia/reperfusion-induced injury along with cardiac functional recovery. Like other vanadium compounds, we documented bis(1-oxy-2-pyridinethiolato) oxovanadium (IV) as a potent cytoprotective agent on myocardial infarction and elicited cardiac functional recovery through activation of Akt signaling pathway.
Results/Conclusion:
The ability of vanadium compounds to activate Akt signaling pathways are responsible for their ability to modulate cardiovascular functions and is probably beneficial as a cardioprotective drug in subjects undergoing reperfusion therapy following myocardial infarction.
Insights
Vanadium compounds, like bis(1-oxy-2-pyridinethiolato) oxovanadium (IV), protect the heart by activating Akt signaling. This pathway enhances survival and recovery after heart attacks, offering potential as a cardioprotective drug.
Area of Science:
- Biochemistry
- Cardiovascular Science
- Pharmacology
Background:
- Akt is a key signaling molecule regulating cell growth, survival, and metabolism.
- Akt activation is a potential therapeutic strategy for increasing cardiomyocyte survival post-ischemia.
Purpose of the Study:
- To investigate the cardioprotective effects of vanadium compounds via Akt signaling.
- To evaluate bis(1-oxy-2-pyridinethiolato) oxovanadium (IV) for myocardial infarction and cardiac functional recovery.
Main Methods:
- Investigated vanadium compounds' mechanism of action on Akt signaling.
- Assessed the cytoprotective and functional recovery effects of a specific vanadium compound in myocardial infarction models.
Main Results:
- Vanadium compounds activate Akt signaling by inhibiting protein tyrosine phosphatases.
- Bis(1-oxy-2-pyridinethiolato) oxovanadium (IV) demonstrated potent cytoprotective effects and improved cardiac function post-myocardial infarction.
- Cardioprotection and functional recovery were linked to Akt signaling pathway activation.
Conclusions:
- Vanadium compounds' ability to activate Akt signaling is crucial for modulating cardiovascular functions.
- These compounds show promise as cardioprotective agents, particularly for patients undergoing reperfusion therapy after myocardial infarction.
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