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Myocardial oxidative stress reduction refers to therapeutic strategies aiming to decrease the level or impact of reactive oxygen species within heart muscle tissue. Oxidative stress is implicated in myocardial injury during infarction and reperfusion, as well as in heart failure and diabetes-related complications. Reducing oxidative stress can prevent or mitigate apoptosis, necrosis, inflammation, and adverse cardiac remodeling. Interventions span a range of drugs (antioxidants, mitochondria-targeted agents, anti-inflammatory agents) that act at various points in the redox regulatory and inflammatory signaling pathways. Appropriate reduction of oxidative stress in myocardial tissue is associated with improved cardiac pump function, reduced incidence of heart failure, and better prognosis following myocardial infarction.
Scavenging of reactive oxygen species; Enhancement of endogenous antioxidant defenses (e.g. glutathione, superoxide dismutase); Inhibition of mitochondrial permeability transition pore opening; Inhibition of apoptosis and autophagy in cardiomyocytes; Attenuation of inflammatory cytokines (e.g., TNF-α, IL-1β, IL-6).
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