Cardiovascular disease is highly prevalent among older adults and poses a huge burden on morbidity, disability, and mortality. The age-related increased vulnerability of the cardiovascular system towards stressors is a pathophysiological trait of cardiovascular disease. This has been associated with a progressive deterioration of blood vessels and decline in heart function during aging. Cardiomyocytes rely mostly on oxidative metabolism for deploying their activities and mitochondrial metabolism is crucial to this purpose. Dysmorphic, inefficient, and oxidant-producing mitochondria have been identified in aged cardiomyocytes in association with cardiac structural and functional alterations. These aberrant organelles are thought to arise from inefficient mitochondrial quality control, which has therefore been place in the spotlight as a relevant mechanism of cardiac aging. As a result of alterations in mitochondrial quality control and redox dyshomeostasis, mitochondrial damage accumulates and contributes to cardiac frailty. Herein, we discuss the contribution of defective mitochondrial quality control pathways to cardiac frailty. Emerging findings pointing towards the exploitation of these pathways as therapeutic targets against cardiac aging and cardiovascular disease will also be illustrated.

心血管疾病在老年人中非常普遍，对发病率、残疾和死亡率构成巨大负担。心血管系统对压力源的年龄相关性增加是心血管疾病的病理生理特征。这与血管逐渐恶化和衰老过程中心脏功能下降有关。心肌细胞主要依靠氧化代谢来展开其活动，而线粒体代谢对此至关重要。已在与心脏结构和功能改变相关的衰老心肌细胞中发现畸形、低效和产生氧化剂的线粒体。这些异常细胞器被认为是由低效的线粒体质量控制引起的，因此，它作为心脏衰老的相关机制而受到关注。由于线粒体质量控制和氧化还原失调的改变，线粒体损伤累积并导致心脏衰弱。在此，我们讨论有缺陷的线粒体质量控制途径对心脏衰弱的贡献。新发现表明将这些途径作为抗心脏衰老和心血管疾病的治疗靶点。