Analysis shows gut microbiota dysbiosis and epigenetic modifications affect myocardial infarction risk, indicating novel therapeutic strategies are needed.
Cardiovascular disease remains the leading cause of morbidity and mortality worldwide, with an increasing incidence despite advances in diagnosis and treatment. Coronary heart disease, particularly acute myocardial infarction, accounts for a significant proportion of cardiovascular deaths. Metabolic imbalances, gut microbiota dysbiosis, and systemic conditions such as obesity and metabolic syndrome contribute to chronic inflammation, endothelial dysfunction, and atherosclerosis progression. This study synthesized evidence from recent clinical and experimental research addressing three main areas: (1) the interplay between gut microbiota dysbiosis, metabolic alterations, and myocardial infarction risk, with emphasis on therapeutic strategies for modulating gut microbiota; (2) the impact of motor neurological disabilities on metabolic regulation and cardiovascular outcomes; and (3) the influence of epigenetic modifications on metabolic pathways relevant to coronary heart disease. Data from proteomic and metabolomic studies were integrated to provide a systems-level perspective. Analysis revealed that gut microbiota dysbiosis promotes systemic inflammation and endothelial dysfunction, amplifying atherosclerotic processes and myocardial infarction risk. Motor neurological impairments were associated with unfavorable metabolic changes that further increase cardiovascular vulnerability. Epigenetic alterations were shown to regulate genes involved in lipid and carbohydrate metabolism, thereby influencing coronary heart disease progression. Proteomics and metabolomics approaches provided comprehensive insights into molecular signatures linking these mechanisms. The integration of microbiome, metabolic, and epigenetic perspectives highlights a complex interplay underlying myocardial infarction risk. Understanding these interactions may enable the development of personalized prevention and treatment strategies, including microbiota-targeted therapies, metabolic modulation, and epigenetic interventions, ultimately contributing to improved cardiovascular outcomes.
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Covali et al. (2025) studied this question.
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