BACKGROUND: Inflammatory bowel disease (IBD), encompassing Crohn's disease and ulcerative colitis, is a chronic relapsing systemic disorder associated with significant extraintestinal manifestations. Emerging evidence indicates that cardiovascular disease represents a clinically important comorbidity in IBD, driven by persistent low-grade inflammation, endothelial dysfunction, and metabolic disturbances. MAIN BODY: The gut microbiota, recognized as a key regulator of host metabolism and immune homeostasis, contributes to cardiovascular physiology through the production of bioactive metabolites. These microbiota-derived metabolites - including short-chain fatty acids, secondary bile acids, trimethylamine N-oxide, tryptophan-derived indoles, and polyphenol-derived compounds - can exert cardioprotective or cardiotoxic effects depending on their balance and bioavailability. In IBD, intestinal dysbiosis and impaired epithelial barrier integrity profoundly alter microbial metabolic output, thereby disrupting systemic inflammatory and cardiovascular pathways. This review summarizes current evidence on the role of microbiota-derived metabolites in cardioprotection and examines how IBD-associated dysbiosis disrupts these protective mechanisms. CONCLUSION: Understanding the interplay between gut dysbiosis and cardiovascular risk in IBD may open new therapeutic avenues. Targeting the gut microbiota and its metabolic output represents a promising strategy to mitigate cardiovascular risk in this patient population.
Olic et al. (2026) studied this question.