摘要
心房颤动(房颤)是临床常见的心律失常,具有高死亡率和致残风险。心房重塑(电、结构重塑)与房颤发病密切相关。成熟心肌细胞向胎儿表型的转换、线粒体功能障碍和活性氧过载的细胞效应等生物学事件参与心房重塑。过氧化物酶体增殖物激活受体(PPAR)是心肌细胞能量代谢调控的关键开关。对房颤能量重塑、心房肌细胞代谢紊乱调控机制的研究,特别是针对PPARγ介导的糖脂代谢表型转换的干预,可能成为房颤治疗的新策略。
Atrial fibrillation is a common arrhythmia with high mortality and disability.Atrial remodeling(electrical and structural remodeling)is closely related to the pathogenesis of atrial fibrillation.Biological events such as the transition of mature cardiomyocytes to fetal phenotype,mitochondrial dysfunction and cellular effects of reactive oxygen species overload are involved in atrial remodeling.Peroxisome proliferator-activated receptor(PPAR)is a key switch in the regulation of energy metabolism in cardiomyocytes.The studies on the regulation mechanism of atrial fibrillation energy remodeling and atrial myocyte metabolic disorder,especially the intervention of glucose and lipid metabolism phenotype switching mediated by PPARγ,may become a new strategy for the treatment of atrial fibrillation.
作者
喜林强
孙华鑫
商鲁翔
汤宝鹏
周贤惠
XI Linqiang;SUN Huaxin;SHANG Luxiang;TANG Baopeng;ZHOU Xianhui(Cardiac Pacing and Electrophysiology/Department of Cardiac Electrophysiology and Remodeling,The First Affiliated Hospital of Xinjiang Medical University,Urumqi 830054,Xinjiang,China)
出处
《心血管病学进展》
CAS
2023年第10期926-929,938,共5页
Advances in Cardiovascular Diseases
基金
国家自然科学基金(82100343,82260065,82260064,82060069)。
关键词
心房颤动
心肌能量代谢
过氧化物酶体增殖物激活受体Γ
线粒体
吡格列酮
Atrial fibrillation
Myocardial energy metabolism
Peroxisome proliferator-activated receptorγ
Mitochondria
Pioglitazone