中国现代医学杂志2025，Vol.35Issue(9)：54-62,9.DOI:10.3969/j.issn.1005-8982.2025.09.009
间歇性低氧干预调节p-STAT3/CPT-1对心肌梗死后小鼠心肌脂肪酸代谢的影响及机制研究
The effect of intermittent hypoxia intervention regulating p-STAT3/CPT-1 on myocardial fatty acid metabolism in mice after myocardial infarction and its mechanism
摘要
Abstract
Objective To investigate the effect of intermittent hypoxia(IH)intervention on myocardial fatty acid metabolism and its mechanism through p-STAT3/CPT-1 regulation in post-myocardial infarction(MI)mice.Methods Thirty-two 6-8-week-old male C57BL6/J mice were randomly divided into four groups(n=8/group):sham-normoxia(SED),sham-IH,MI-normoxia(MI-SED),and MI-IH.MI was induced by left anterior descending coronary artery ligation.After 1-week recovery,IH groups received 4 h/day,5 days/week hypoxia(simulated 5 000 m altitude,13%O₂)for 4 weeks.We assessed body weight,exercise tolerance,left ventricular ejection fraction(LVEF),myocardial fibrosis,mitochondrial ultrastructure,ATP content,citrate synthase(CS)activity,and protein expression(CD36,LCAD,ACOX1,p-STAT3,CPT1)Results Compared with MI-SED,MI-IH showed:improved exercise tolerance(P<0.05),increased LVEF(P<0.05),reduced fibrosis(P<0.05),preserved mitochondrial structure,elevated ATP(P<0.05)and CS activity(P<0.05).Fatty acid oxidation proteins(CD36,LCAD,ACOX1)and p-STAT3 expression increased significantly.Both protein and gene expression of CPT1 were upregulated(all P<0.05).Conclusion IH improves post-MI cardiac function by enhancing fatty acid oxidation via p-STAT3/CPT-1 pathway,preserving mitochondrial integrity and reducing fibrosis.关键词
心肌梗死/间歇性低氧干预/脂肪酸代谢/线粒体/心脏康复Key words
myocardial infarction/intermittent hypoxia intervention/fatty acid metabolism/mitochondria/cardiac rehabilitation分类
医药卫生引用本文复制引用
闫馨月,黄传,江玉娟,万春晓..间歇性低氧干预调节p-STAT3/CPT-1对心肌梗死后小鼠心肌脂肪酸代谢的影响及机制研究[J].中国现代医学杂志,2025,35(9):54-62,9.基金项目
天津市医学重点学科(专业)建设项目(No:TJYXZDXK-060B) （专业）
"双一流"学科建设项目(No:TJWJ2022XK007) （No:TJWJ2022XK007）
天津市卫生健康科技项目(No:TJWJ2023QN008) （No:TJWJ2023QN008）
