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摘要：
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摘要：代谢相关脂肪性肝病（metabolic dysfunction-associated steatotic liver disease，
MASLD）已成为全球最常见的慢性肝病，其发病率与肥胖、2型糖尿病、高血压等心脏
代谢危险因素密切相关。近年来大量研究表明，MASLD的危害并非局限于肝脏本身，还
与心血管疾病（cardiovascular disease，CVD）存在显著联系，二者在病理生理机制上共享
多条路径，包括慢性低度炎症、胰岛素抵抗、内皮功能障碍和氧化应激等。MASLD患者
罹患动脉粥样硬化、冠心病，心力衰竭和心律失常的风险显著升高；与此同时，CVD亦
可通过影响共同代谢机制、交感神经系统和血流动力学进一步加重肝脏炎症与纤维化的
进展。因此，MASLD与CVD并非彼此独立，心肝间的密切关联构成了重要的临床课题。
尽管MASLD与CVD具有高度交叉的病理基础与临床风险，在当前临床实践中，脂肪性肝
病患者的管理在肝病科与心血管科往往缺乏系统合作，导致MASLD患者早期筛查不足，
治疗路径碎片化。本综述聚焦于MASLD与CVD间的双向关联，梳理其共同的发病机制与
相互影响的临床证据，强调代谢综合管理的重要性，并提出通过生活方式干预和危险因
素控制（如体质量、血糖、血脂）改善疾病结局的策略。未来应推动基于MASLD视角的
CVD风险识别与管理模式，为代谢相关慢性疾病的综合防控提供新路径。
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Abstract: Metabolic dysfunction-associated steatotic liver disease (MASLD) has emerged as the
most prevalent chronic liver disease globally, with its incidence closely linked to cardiometabolic
risk factors such as obesity, type 2 diabetes and hypertension. Recent extensive research revealed
that the impact of MASLD extended beyond liver itself, demonstrating significant bidirectional
associations with cardiovascular disease (CVD). These conditions shared multiple intertwined
pathophysiological pathways, including chronic low-grade inflammation, insulin resistance,
endothelial dysfunction and oxidative stress. Patients with MASLD exhibited a markedly elevated
risk of developing atherosclerosis, coronary heart disease, heart failure and arrhythmias. Conversely,
CVD could further exacerbate hepatic inflammation and fibrosis progression by disrupting shared
metabolic mechanisms, activating the sympathetic nervous system, and altering hemodynamics.
Thus, MASLD and CVD were not mutually exclusive but interconnected, presenting a significant
clinical challenge. Despite the highly overlapping pathological foundations and clinical risks
between MASLD and CVD, current clinical practice often lacked systematic collaboration between
hepatology and cardiology departments. This fragmentation resulted in inadequate early screening
for MASLD patients and disjointed treatment pathways. This review focused on the bidirectional
relationship between MASLD and CVD, delineated their shared pathogenic mechanisms and
clinical evidence of mutual influence, and underscored the imperative for integrated metabolic
management. We proposed strategies centered on lifestyle interventions and rigorous control of
metabolic risk factors (e.g., weight, blood glucose, lipids) to improve disease outcomes. Moving
forward, it was essential to advance CVD risk identification and management models from an
MASLD perspective, offering novel paradigms for the comprehensive prevention and control of
metabolism-related chronic diseases.
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