Early myocardial ischemia and hypoxia trigger compensatory mechanisms, but prolonged hypoxic damage increases pro-inflammatory cytokines (IL-1β, IL-6, and TNF-α) and reactive species (O2·−, ·OH, and H2O2), and shifts metabolism from fatty acid oxidation to glycolysis, further worsening cardiac hypertrophy, myocarditis, and heart failure (Adzika et al., 2023; Ndzie Noah et al., 2024). The gene discussed is IL1B; the disease is cardiac hypertrophy.