线粒体分裂
线粒体融合
线粒体
肥胖
生物信息学
医学
生物
活力
细胞生物学
内科学
线粒体DNA
遗传学
物理
量子力学
基因
作者
Chayodom Maneechote,Nipon Chattipakorn,Nipon Chattipakorn
出处
期刊:Life Sciences
[Elsevier]
日期:2024-05-01
卷期号:344: 122575-122575
标识
DOI:10.1016/j.lfs.2024.122575
摘要
Increasing global obesity rates and an aging population are independently linked to cardiac complications. Consequently, it is crucial to comprehensively understand the mechanisms behind these conditions to advance innovative therapies for age-related diseases. Mitochondrial dysfunction, specifically defects in mitochondrial fission/fusion processes, has emerged as a central regulator of cardiac complications in aging and age-related diseases (e.g., obesity). Since excessive fission and impaired fusion of cardiac mitochondria lead to disruptions in mitochondrial dynamics and cellular metabolism in aging and obesity, modulating mitochondrial dynamics with either fission inhibitors or fusion promoters has offered cardioprotection against these pathological conditions in preclinical models. This review explores the molecular mechanisms governing mitochondrial dynamics as well as the disturbances observed in aging and obesity. Additionally, pharmaceutical interventions that specifically target the processes of mitochondrial fission and fusion are presented and discussed. By establishing a connection between mitochondrial dynamism through fission and fusion and the advancement or mitigation of age-related diseases, particularly obesity, this review provides valuable insights into the progression and potential prevention strategies for such conditions.
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