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.

中文翻译：

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关于心脏线粒体动力学在肥胖和衰老中的作用的未来展望

全球肥胖率上升和人口老龄化与心脏并发症独立相关。因此，全面了解这些疾病背后的机制对于推进年龄相关疾病的创新疗法至关重要。线粒体功能障碍，特别是线粒体裂变/融合过程的缺陷，已成为衰老和年龄相关疾病（例如肥胖）心脏并发症的核心调节因子。由于心脏线粒体的过度裂变和融合受损会导致衰老和肥胖过程中线粒体动力学和细胞代谢的破坏，因此用裂变抑制剂或融合促进剂调节线粒体动力学已在临床前模型中针对这些病理状况提供了心脏保护作用。这篇综述探讨了控制线粒体动力学的分子机制以及在衰老和肥胖中观察到的紊乱。此外，还介绍并讨论了专门针对线粒体裂变和融合过程的药物干预措施。通过通过裂变和融合建立线粒体活力与年龄相关疾病（特别是肥胖症）的进展或减轻之间的联系，这篇综述为此类疾病的进展和潜在预防策略提供了宝贵的见解。