Gut-heart axis disruption and LPS translocation: driving atrial fibrillation through inflammatory storm and fibrotic mechanisms

Atrial fibrillation (AF) is one of the most prevalent arrhythmias in clinical practice, posing a significant threat to human health. The gut microbiota and its metabolites exert crucial effects on cardiovascular diseases via the gut-heart axis. Lipopolysaccharide (LPS), a component of Gram-negative bacterial cell walls, can enter the bloodstream when intestinal barrier function is compromised, triggering systemic inflammatory responses. Recent studies indicate that elevated LPS levels may increase the risk of AF onset through mechanisms such as promoting inflammation, oxidative stress, and myocardial fibrosis, and are associated with AF recurrence and poor prognosis. This review examines the role and mechanisms of LPS in the development and progression of AF, and explores potential strategies for preventing and treating AF by reducing LPS levels through approaches including gut microbiota modulation, anti-inflammatory diets, targeted inhibitors, and traditional Chinese medicine therapies.