Headley Colwyn A, Tsao Philip S
Stanford Cardiovascular Institute, Stanford University School of Medicine, Stanford, CA, United States.
Front Cardiovasc Med. 2023 May 9;10:1141124. doi: 10.3389/fcvm.2023.1141124. eCollection 2023.
Mitochondrial dysfunction is a common denominator in both biological aging and cardiovascular disease (CVD) pathology. Understanding the protagonist role of mitochondria in the respective and independent progressions of CVD and biological aging will unravel the synergistic relationship between biological aging and CVD. Moreover, the successful development and implementation of therapies that can simultaneously benefit mitochondria of multiple cell types, will be transformational in curtailing pathologies and mortality in the elderly, including CVD. Several works have compared the status of mitochondria in vascular endothelial cells (ECs) and vascular smooth muscle cells (VSMCs) in CVD dependent context. However, fewer studies have cataloged the aging-associated changes in vascular mitochondria, independent of CVD. This mini review will focus on the present evidence related to mitochondrial dysfunction in vascular aging independent of CVD. Additionally, we discuss the feasibility of restoring mitochondrial function in the aged cardiovascular system through mitochondrial transfer.
线粒体功能障碍是生物衰老和心血管疾病（CVD）病理过程的一个共同特征。了解线粒体在CVD和生物衰老各自独立进展过程中的主角作用，将揭示生物衰老与CVD之间的协同关系。此外，成功开发并实施能够同时惠及多种细胞类型线粒体的疗法，将在减少包括CVD在内的老年人病理状况和死亡率方面带来变革。有几项研究比较了在依赖CVD的背景下血管内皮细胞（ECs）和血管平滑肌细胞（VSMCs）中线粒体的状态。然而，较少有研究对与衰老相关的血管线粒体变化进行分类，且不考虑CVD因素。本综述将聚焦于与不依赖CVD的血管衰老中线粒体功能障碍相关的现有证据。此外，我们还将讨论通过线粒体转移恢复老年心血管系统线粒体功能的可行性。
