Arterial aging: a journey into subclinical arterial disease.
Arterial aging: a journey into subclinical arterial disease.
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DOI：
10.1097/mnh.0b013e3283361c0b
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发表时间：
2010-03
影响因子：
3.2
通讯作者：
Lakatta EG
中科院分区：
文献类型：
--
作者：
Wang M;Monticone RE;Lakatta EG
细胞、基质和生物分子中与年龄相关的动脉变化是老年人心血管疾病发生和进展的基础。本综述重点关注细胞和分子水平上动脉壁内衰老与疾病相互交织的最新进展。内皮功能障碍、VSMC 增殖/侵入/分泌、基质破碎、胶原化和糖化是与年龄相关的动脉表型的特征，为动脉疾病的发病机制创造了富含活性氧 (ROS) 的微环境。这个生态位创造了一种与年龄相关的动脉分泌表型（AAASP），它是由许多年龄修饰的 Ang II 信号分子的协同作用精心策划的。大多数构成 AASP 的生物分子、细胞和基质修饰可以由年轻时的实验性高血压或动脉粥样硬化引起。动脉 AAASP 还具有其他间充质细胞（即成纤维细胞）中发现的衰老相关分泌表型 (SASP) 的特征。亚临床 AAASP 在衰老过程中不断演变。针对这种亚临床 AAASP 可能会减少典型的与年龄相关的动脉疾病（即高血压和动脉粥样硬化）的发病率和进展。
Age-associated arterial alterations in cells, matrix, and biomolecules are the foundation for the initiation and progression of cardiovascular diseases in older persons. This review focuses on the latest advances on the intertwining of aging and disease within the arterial wall at the cell and molecular levels. Endothelial dysfunction, VSMC proliferation/invasion/secretion, matrix fragmentation, collagenization and glycation are characteristics of an age-associated arterial phenotype that creates a microenvironment enriched with reactive oxygen species (ROS) for the pathogenesis of arterial disease. This niche creates an age-associated arterial secretory phenotype (AAASP), which is orchestrated by the concerted effects of numerous age-modified Ang II signaling molecules. Most of these biomolecular, cell, and matrix modifications that comprise the AASP can be elicited by experimental hypertension or atherosclerosis at a younger age. The arterial AAASP also shares features of a senescence associated secretory phenotype (SASP) identified in other mesenchymocytes, i.e. fibroblasts. A subclinical AAASP evolves during aging. Targeting this subclinical AAASP may reduce the incidence and progression of the quintessential age-associated arterial diseases, i.e. hypertension and atherosclerosis.