Gut microecology and cardiovascular disease: core pathogenic mechanisms and clinical intervention strategies.

Abstract

Cardiovascular diseases (CVDs) remain a leading cause of morbidity and mortality worldwide, and their burden continues to rise. The gut microbiota is a key interface linking host metabolism, environmental exposures, and immunity, and accumulating evidence implicates gut dysbiosis in the pathogenesis, progression, and clinical outcomes of CVDs. Dysbiosis may promote the pathological "gut-heart axis" by impairing intestinal barrier integrity, amplifying systemic inflammation, disrupting metabolic homeostasis, and altering immune networks. Microbiota-targeted strategies-including dietary modulation and physical activity, probiotics and prebiotics, fecal microbiota transplantation (FMT), and microbial enzyme or metabolite inhibitors-have yielded promising preclinical results and early clinical signals; however, long-term efficacy, safety, and patient-selection criteria remain uncertain. This review synthesizes evidence on gut microbial alterations and major metabolites, including trimethylamine N-oxide (TMAO), short-chain fatty acids (SCFAs), and lipopolysaccharide (LPS), across atherosclerosis, acute coronary syndrome, hypertension, ischemic heart disease, and heart failure. We compare disease-specific mechanisms, critically appraise therapeutic evidence and safety, and identify priorities for causal, standardized, and clinically meaningful research. These findings provide a mechanistic framework for microbiome-informed prevention and adjunctive management of CVD while emphasizing that microbiota-directed interventions should not replace guideline-directed care.