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Glutathione "Redox Homeostasis" and Its Relation to Cardiovascular Disease
Vladan P Bajic1, Christophe Van Neste2, Milan Obradovic1
1Laboratory for Radiobiology and Molecular Genetics, Institute of Nuclear Sciences Vinca, University of Belgrade, Mike Petrovica Alasa 12-14, 11000 Belgrade, Serbia.
Insights
Cardiovascular diseases (CVD) arise from impaired redox homeostasis. Both excessive oxidative stress (OS) and reductive stress (RS) disrupt this balance, impacting heart health and leading to cardiac dysfunction.
Area of Science:
- Biochemistry
- Cardiology
- Cellular Biology
Background:
- Cardiovascular diseases (CVD) are the leading cause of mortality worldwide.
- Cardiovascular complications are linked to an imbalance in "redox homeostasis," involving oxidative stress (OS) and reductive stress (RS).
Purpose of the Study:
- To review experimental findings on the role of redox homeostasis in cardiovascular complications.
- To examine the specific involvement of glutathione in altered redox states within the heart.
Main Methods:
- Compilation and analysis of existing experimental research findings.
- Focus on studies investigating glutathione's role in cardiac redox balance.
Main Results:
- Sustained shifts towards OS or RS disrupt the homeostatic redox mechanism, contributing to cardiovascular complications.
- Impaired redox homeostasis, particularly involving glutathione, can impair cellular signaling and increase proteotoxicity.
Conclusions:
- Both oxidative and reductive stress contribute to cardiovascular complications by disrupting redox homeostasis.
- Glutathione plays a critical role in maintaining cardiac redox balance, and its dysfunction under OS or RS leads to cardiac dysfunction.
Abstract:
More people die from cardiovascular diseases (CVD) than from any other cause. Cardiovascular complications are thought to arise from enhanced levels of free radicals causing impaired "redox homeostasis," which represents the interplay between oxidative stress (OS) and reductive stress (RS). In this review, we compile several experimental research findings that show sustained shifts towards OS will alter the homeostatic redox mechanism to cause cardiovascular complications, as well as findings that show a prolonged antioxidant state or RS can similarly lead to such cardiovascular complications. This experimental evidence is specifically focused on the role of glutathione, the most abundant antioxidant in the heart, in a redox homeostatic mechanism that has been shifted towards OS or RS. This may lead to impairment of cellular signaling mechanisms and elevated pools of proteotoxicity associated with cardiac dysfunction.
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