Yang Bojun, Xu Jiahao, Dao Xiaoyan, Huang Yu, Liang Jiling, Huang Jielun, Gou Bo, Yan Hanyu, Chen Ning, Fan Jingjing
Hubei Key Laboratory of Exercise Training and Monitoring, College of Sports Medicine, Wuhan Sports University, Wuhan 430079, China.
Int J Mol Sci. 2025 May 21;26(10):4935. doi: 10.3390/ijms26104935.
Obesity cardiomyopathy (OCM) represents a rapidly growing health concern globally, characterized by metabolic, structural, and functional abnormalities of the heart. Current research has demonstrated that inflammation plays a pivotal role in obesity-induced cardiomyopathy, and that regular exercise can ameliorate lipid disturbances and inflammatory abnormalities effectively. However, the underlying mechanisms are not fully elucidated. We investigated the effects of an 8-week aerobic exercise intervention on myocardial structure, function, and inflammation in HFD-induced obese mice. The results revealed that aerobic exercise alleviated myocardium pyroptosis and inflammation by down-regulating the PI3K/AKT signaling pathway. Furthermore, the inhibition of the PI3K pathway by LY294002, coupled with exercise, attenuated and suppressed HFD-induced myocardial impairments, inflammation, and pyroptosis, with a synergistic effect. Based on these findings, we concluded that eight weeks of aerobic exercise synergizes with the inhibition of PI3K through inflammatory and pyroptosis mechanisms to improve obesity-associated myocardial remodeling and dysfunction. Therefore, long-term regular aerobic exercise represents a potential strategy in the treatment of OCM.
肥胖性心肌病（OCM）是全球范围内一个迅速增长的健康问题，其特征为心脏的代谢、结构和功能异常。目前的研究表明，炎症在肥胖诱导的心肌病中起关键作用，且规律运动可有效改善脂质紊乱和炎症异常。然而，其潜在机制尚未完全阐明。我们研究了为期8周的有氧运动干预对高脂饮食诱导的肥胖小鼠心肌结构、功能和炎症的影响。结果显示，有氧运动通过下调PI3K/AKT信号通路减轻了心肌细胞焦亡和炎症。此外，LY294002对PI3K通路的抑制与运动相结合，减轻并抑制了高脂饮食诱导的心肌损伤、炎症和细胞焦亡，具有协同作用。基于这些发现，我们得出结论，为期8周的有氧运动通过炎症和细胞焦亡机制与PI3K抑制协同作用，改善肥胖相关的心肌重塑和功能障碍。因此，长期规律的有氧运动是治疗OCM的一种潜在策略。
