Picos Aitor, Seoane Nuria, Campos-Toimil Manuel, Viña Dolores
Physiology and Pharmacology of Chronic Diseases (FIFAEC), Center for Research in Molecular Medicine and Chronic Diseases (CiMUS), University of Santiago de Compostela, 15782, Santiago de Compostela, Spain.
Translational Research in Neurological Diseases (ITEN), Health Research Institute of Santiago de Compostela (IDIS), USC University Hospital Complex (CHUS), SERGAS, Santiago de Compostela, Spain.
Biogerontology. 2025 May 26;26(3):118. doi: 10.1007/s10522-025-10256-5.
The aging vasculature is characterized by endothelial dysfunction, arterial stiffness, and increased susceptibility to vascular pathologies. Central to these changes is the process of cellular senescence, where endothelial and vascular smooth muscle cells lose their replicative and functional capacity and adopt a pro-inflammatory secretory phenotype. This review provides an overview of the key mechanisms underlying vascular senescence, including the p53/p21 and p16/Rb pathways, the senescence-associated secretory phenotype (SASP), and oxidative stress, examines its contribution to cardiovascular diseases in older adults, and highlights emerging therapeutic strategies aimed at delaying or reversing these age-related vascular changes. In vascular cells, DNA damage, oxidative stress, and chronic inflammation associated with aging converge to amplify senescence. Clinically, vascular senescence is linked with hypertension, atherosclerosis, and increased overall cardiovascular risk. Several interventions, ranging from senolytics to lifestyle factors, show promise in mitigating these changes; however, long-term studies are needed. Given that vascular senescence is a pivotal driver of cardiovascular pathology in aging, targeting senescent cells or their secretory phenotype may potentially offer new avenues for preventing or attenuating age-related vascular diseases. This review presents an updated and integrative overview of vascular senescence, connecting fundamental cellular mechanisms with their clinical manifestations and highlighting the most promising therapeutic interventions.
衰老的血管系统具有内皮功能障碍、动脉僵硬以及对血管病变易感性增加等特征。这些变化的核心是细胞衰老过程，在此过程中，内皮细胞和血管平滑肌细胞丧失其复制和功能能力，并呈现促炎分泌表型。本综述概述了血管衰老的关键机制，包括p53/p21和p16/Rb通路、衰老相关分泌表型（SASP）以及氧化应激，探讨了其对老年人心血管疾病的影响，并重点介绍了旨在延缓或逆转这些与年龄相关的血管变化的新兴治疗策略。在血管细胞中，与衰老相关的DNA损伤、氧化应激和慢性炎症相互作用，加剧了细胞衰老。在临床上，血管衰老与高血压、动脉粥样硬化以及整体心血管风险增加有关。从衰老细胞溶解剂到生活方式因素等多种干预措施，在减轻这些变化方面显示出前景；然而，仍需要长期研究。鉴于血管衰老在衰老过程中是心血管病理的关键驱动因素，靶向衰老细胞或其分泌表型可能为预防或减轻与年龄相关的血管疾病提供新途径。本综述对血管衰老进行了更新和综合概述，将基本细胞机制与其临床表现相联系，并突出了最有前景的治疗干预措施。
