代谢功能障碍相关脂肪性肝病(MASLD)与心血管疾病(CVD)的共病进展由肠道微生态失衡驱动。肠道菌群及其代谢谱
在不良生活方式与遗传易感性作用下发生病理性重构，通过短链脂肪酸减少、胆汁酸池重置及有害代谢物累积，破坏肠屏障完整性并引发代谢性内毒素血症，进而触发肝脏代谢重构与炎症级联反应。受损肝脏释放的病理性肝源性因子与肠源性信号协同，诱导骨髓训练免疫及系统性炎症浸润，共同驱动内皮功能障碍、动脉粥样硬化及心肌重塑。此外，心衰导致的静脉淤血与肠道低灌注可反向加重肠漏，形成恶性反馈环。基于肠-肝-心轴的干预策略，如微生态调节及靶向代谢通路的小分子药物，展现出跨器官防治潜力。未来需整合多组学与纵向队列构建基于微生物特征的精准分层模型，以实现MASLD–CVD共病的个体化诊疗。

Gut dysbiosis appears to be a central driver of metabolic dysfunction-associated steatotic liver disease (MASLD) and cardiovascular disease (CVD) comorbidity. Under diet, lifestyle, and host genetic constraints, the microbiome shifts toward a metabolite profile marked by lower short-chain fatty acids, an imbalanced bile-acid pool, and accumulation of detrimental microbial products. The resulting loss of barrier integrity facilitates metabolic endotoxemia and sets off hepatic metabolic rewiring with inflammatory amplification. Liver-derived mediators then interact with gut signals to promote trained immunity in the bone marrow and sustain systemic inflammation, contributing to endothelial dysfunction, atherogenesis, and cardiac remodeling. Importantly, impaired cardiac function feeds back on the gut: congestion and hypoperfusion worsen permeability and intensify dysbiosis, creating a vicious cycle. Targeting the gut–liver–heart axis using microbiota modulators or drugs aimed at specific pathways could therefore yield coordinated benefits across organs. Future work should combine multi-omics with longitudinal sampling to derive microbiomebased stratification tools for precision management of MASLD with CVD.