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

## TL;DR

This paper explores how gut-heart axis disruption and LPS translocation contribute to atrial fibrillation through inflammation and fibrosis, and suggests potential treatment strategies.

## Contribution

The paper reviews novel mechanisms linking gut microbiota disruption and LPS to atrial fibrillation and proposes new therapeutic approaches.

## Key findings

- Elevated LPS levels are linked to atrial fibrillation onset through inflammation and fibrosis.
- Gut microbiota modulation and anti-inflammatory diets may help prevent or treat atrial fibrillation.
- Traditional Chinese medicine and TLR4 inhibitors are potential therapeutic strategies.

## Abstract

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.

Diagram illustrating gut dysbiosis leading to a leaky gut and endotoxemia, which triggers chronic inflammation, oxidative stress, myocardial fibrosis, and autonomic dysfunction, ultimately contributing to atrial fibrillation; possible interventions shown include probiotics, colchicine, anti-inflammatory diet, TLR4 inhibitors, and traditional Chinese medicine.