Evans Department of Medicine and Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, MA 02118, USA.
Department of Pediatric Surgery, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA.
Int J Mol Sci. 2024 Oct 17;25(20):11188. doi: 10.3390/ijms252011188.
Vascular aging encompasses structural and functional changes in the vasculature, significantly contributing to cardiovascular diseases, which are the leading cause of death globally. The incidence and prevalence of these diseases increase with age, with most morbidity and mortality attributed to myocardial infarction and stroke. Diagnosing and intervening in vascular aging while understanding the mechanisms behind age-induced vascular phenotypic and pathophysiological alterations offers the potential for delaying and preventing cardiovascular mortality in an aging population. This review delves into various aspects of vascular aging by examining age-related changes in arterial health at the cellular level, including endothelial dysfunction, cellular senescence, and vascular smooth muscle cell transdifferentiation, as well as at the structural level, including arterial stiffness and changes in wall thickness and diameter. We also explore aging-related changes in perivascular adipose tissue deposition, arterial collateralization, and calcification, providing insights into the physiological and pathological implications. Overall, aging induces phenotypic changes that augment the vascular system's susceptibility to disease, even in the absence of traditional risk factors, such as hypertension, diabetes, obesity, and smoking. Overall, age-related modifications in cellular phenotype and molecular homeostasis increase the vulnerability of the arterial vasculature to structural and functional alterations, thereby accelerating cardiovascular risk. Increasing our understanding of these modifications is crucial for success in delaying or preventing cardiovascular diseases. Non-invasive techniques, such as measuring carotid intima-media thickness, pulse wave velocity, and flow-mediated dilation, as well as detecting vascular calcifications, can be used for the early detection of vascular aging. Targeting specific pathological mechanisms, such as cellular senescence and enhancing angiogenesis, holds promise for innovative therapeutic approaches.
血管衰老涵盖了血管的结构和功能变化,对心血管疾病有重大影响,而心血管疾病是全球死亡的主要原因。这些疾病的发病率和患病率随着年龄的增长而增加,大多数发病率和死亡率归因于心肌梗死和中风。诊断和干预血管衰老,同时了解年龄引起的血管表型和病理生理改变的机制,为延迟和预防老龄化人口的心血管死亡率提供了潜力。
这篇综述通过研究细胞水平上动脉健康的与年龄相关的变化,包括内皮功能障碍、细胞衰老和血管平滑肌细胞转分化,以及结构水平上的动脉僵硬和壁厚度和直径的变化,深入探讨了血管衰老的各个方面。我们还探讨了与年龄相关的血管周围脂肪组织沉积、动脉侧支形成和钙化的变化,深入了解其生理和病理意义。
总的来说,衰老会引起表型变化,增加血管系统对疾病的易感性,即使在没有高血压、糖尿病、肥胖和吸烟等传统危险因素的情况下也是如此。总之,细胞表型和分子动态平衡的年龄相关性改变增加了动脉血管结构和功能改变的脆弱性,从而加速了心血管风险。
增加我们对这些改变的理解对于成功延迟或预防心血管疾病至关重要。非侵入性技术,如测量颈动脉内膜中层厚度、脉搏波速度和血流介导的扩张,以及检测血管钙化,可用于早期发现血管衰老。针对特定的病理机制,如细胞衰老和增强血管生成,为创新的治疗方法提供了希望。