氧化应激
肥厚性心肌病
活性氧
医学
肌酸激酶
内科学
线粒体
心肌病
氧化磷酸化
内分泌学
药理学
心脏病学
缺血
舒张期
心脏病
心源性猝死
肌球蛋白
横纹肌溶解症
肌钙蛋白
高能
心脏功能不全
能量代谢
再灌注损伤
作者
Anton Xu,David Weissman,Katharina J. Ermer,Edoardo Bertero,Jan M. Federspiel,Felix Stadler,Elisa Grünler,Melina Tangos,Sevasti Zervou,Mark T. Waddingham,James T. Pearson,Jan‐Christian Reil,Smita Scholtz,Jan Dudek,Michael Kohlhaas,Alexander Nickel,Lucie Carrier,Thomas Eschenhagen,Michelle Michels,Cristobal G. dos Remedios
出处
期刊:Circulation
[Lippincott Williams & Wilkins]
日期:2025-10-20
卷期号:152 (24): 1705-1727
被引量:3
标识
DOI:10.1161/circulationaha.125.074120
摘要
This study reveals a mechanistic link between hypercontractility, mitochondrial reactive oxygen species, and CK dysfunction in HCM, perpetuating a cycle of energetic dysfunction. Targeting hypercontractility and oxidative stress through myosin inhibition offers a strategy to restore energy balance and reduce arrhythmic risk in HCM.
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