Cardiac aging involves progressive structural, functional, cellular, and molecular changes that impair heart function. This review explores key mechanisms, including oxidative stress, mitochondrial dysfunction, impaired autophagy, and chronic low-grade inflammation. Excess reactive oxygen species (ROS) damage heart muscle cells, contributing to fibrosis and cellular aging. Mitochondrial dysfunction reduces energy production and increases oxidative stress, accelerating cardiac decline. Impaired autophagy limits the removal of damaged proteins and organelles, while inflammation activates signaling molecules that drive tissue remodeling. Gender differences reveal estrogen's protective role in premenopausal women, with men showing greater susceptibility to heart muscle dysfunction and injury. After menopause, women lose this hormonal protection, increasing their risk of cardiovascular conditions. Ethnic disparities, particularly among underserved minority populations, emphasize how social factors such as access to care, environment, and chronic stress contribute to worsening cardiovascular outcomes. The coronavirus disease pandemic has introduced further challenges by increasing the incidence of heart damage through inflammation, blood clots, and long-term heart failure, especially in older adults with existing metabolic conditions like diabetes and high blood pressure. The virus's interaction with receptors on heart and blood vessel cells, along with a weakened immune response in older adults, intensifies cardiac aging. Emerging therapies include delivery of therapeutic extracellular vesicles, immune cell modulation, and treatments targeting mitochondria. In addition, lifestyle strategies such as regular physical activity, nutritional improvements, and stress reduction remain vital to maintaining cardiac health. Understanding how these biological and social factors intersect is critical to developing targeted strategies that promote healthy aging of the heart.

Keywords: COVID-19 cardiovascular complications; cardiac aging; health disparities; mitochondrial dysfunction; oxidative stress.

心脏老化涉及渐进性的结构、功能、细胞和分子变化，这些变化会损害心肌功能。本综述探讨了关键机制，包括氧化应激、线粒体功能障碍、自噬受损以及慢性低级别炎症。过多的活性氧（ROS）会损伤心肌细胞，导致纤维化和细胞衰老。线粒体功能障碍减少了能量产生并增加了氧化应激，从而加速心脏衰退。自噬受损限制了损坏蛋白质和细胞器的清除能力，而炎症则激活了驱动组织重塑的信号分子。性别差异揭示雌激素在绝经前女性中的保护作用，男性对心肌功能障碍和损伤更易感。绝经后，女性丧失这种荷尔蒙保护，增加了心血管疾病的风险。种族差异，特别是在服务不足的少数族裔群体中，强调了社会因素如医疗资源获取、环境以及长期压力如何导致心血管状况恶化。冠状病毒病大流行通过炎症、血栓和长期心力衰竭进一步增加了心脏损伤的发生率，尤其是对于患有糖尿病和高血压等代谢性疾病的老年患者。该病毒与心肌和血管细胞上的受体相互作用，并且老年患者的免疫反应较弱，加剧了心脏老化过程。新兴的治疗方案包括递送治疗性胞外囊泡、调节免疫细胞以及针对线粒体进行靶向治疗。此外，生活方式策略如定期体育活动、营养改善和压力减少对于保持心脏健康仍然至关重要。理解这些生物学和社会因素如何相互作用对于开发促进心脏健康老化的针对性策略是至关重要的。

关键词：Covid-19心血管并发症；心脏老化；健康差异；线粒体功能障碍；氧化应激。