温州医科大学林灼锋小组的一项最新研究的研究显示，心肌梗死通过触发免疫炎症反应和诱导骨膜炎加速MASH的进展。相关论文于2024年6月4日发表于国际顶尖学术期刊《细胞—代谢》杂志上。

据介绍，代谢功能障碍相关脂肪性肝病(MASLD)患者，特别是晚期代谢功能障碍相关脂肪性肝炎(MASH)患者，患心血管疾病(CVDs)的风险增加。心血管疾病是否会反过来影响代谢功能障碍相关脂肪性肝病的发病机制仍然未知。

研究组发现心肌梗死(MI)加速了代谢功能障碍相关脂肪性肝病的肝脏病理进展。在诊断后经历心血管疾病的代谢功能障碍相关脂肪性肝病患者中，表现出加速的肝纤维化进展。心肌梗死促进代谢功能障碍相关脂肪性肝炎小鼠肝纤维化，伴有循环Ly6C^hi单核细胞升高及其向受损肝组织的募集。当删除这些细胞时，这些副作用被显著地消除了。

同时，心肌梗死显著增加循环和心脏骨膜蛋白水平，其作用于肝细胞和星状细胞，促进肝脏脂质积累和纤维化，最终加剧肝脏相关脂肪性肝炎的病理进展。这些临床前和临床结果表明，心肌梗死改变了系统稳态，上调了促纤维化因子的产生，引发了加速代谢功能障碍相关脂肪性肝病病理进展的跨疾病通讯。

附：英文原文

Title: Myocardial infarction accelerates the progression of MASH by triggering immuno inflammatory response and induction of periosti

Author: Wei Xie, Jing Gan, Xiaodong Zhou, Huiying Tian, Xingchao Pan, Wenyue Liu, Xiaokun Li, Jie Du, Aimin Xu, Minghua Zheng, Fan Wu, Yuling Li, Zhuofeng Lin

Issue&Volume: 2024/06/04

Abstract: Patients with metabolic dysfunction-associated steatotic liver disease (MASLD), especiallyadvanced metabolic dysfunction-associated steatohepatitis (MASH), have an increasedrisk of cardiovascular diseases (CVDs). Whether CVD events will, in turn, influencethe pathogenesis of MASLD remains unknown. Here, we show that myocardial infarction(MI) accelerates hepatic pathological progression of MASLD. Patients with MASLD whoexperience CVD events after their diagnosis exhibit accelerated liver fibrosis progression.MI promotes hepatic fibrosis in mice with MASH, accompanied by elevated circulatingLy6Chi monocytes and their recruitment to damaged liver tissues. These adverse effects aresignificantly abrogated when deleting these cells. Meanwhile, MI substantially increasescirculating and cardiac periostin levels, which act on hepatocytes and stellate cellsto promote hepatic lipid accumulation and fibrosis, finally exacerbating hepatic pathologicalprogression of MASH. These preclinical and clinical results demonstrate that MI alterssystemic homeostasis and upregulates pro-fibrotic factor production, triggering cross-diseasecommunication that accelerates hepatic pathological progression of MASLD.

DOI: 10.1016/j.cmet.2024.04.020

Source: https://www.cell.com/cell-metabolism/abstract/S1550-4131(24)00176-1