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Early myocardial ischemia and hypoxia trigger compensatory mechanisms, but prolonged hypoxic damage increases pro-inflammatory cytokines (IL-1, IL-6, and TNF-) and reactive species (O2, OH, and H2O2), and shifts metabolism from fatty acid oxidation to glycolysis, further worsening cardiac hypertrophy, myocarditis, and heart failure ( + /NADH ratio, oxidative stress, and kinetics
The lysosome as a command-and-control center for cellular metabolism
More research is required in the future to elucidate how semaglutide may be having these effects
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