Division of Geriatric Medicine and Gerontology, Johns Hopkins University School of Medicine, John R. Burton Pavilion, 5505 Hopkins Bayview Circle, Baltimore, MD 21224, USA.
Clin Geriatr Med. 2011 Feb;27(1):53-65. doi: 10.1016/j.cger.2010.08.004.
Over the last few decades, the understanding of the renin-angiotensin system (RAS) has advanced dramatically. RAS is now thought to play a crucial role in physiologic and pathophysiologic mechanisms in almost every organ system and is a key regulator of hypertension, cardiovascular disease, and renal function. Angiotensin II (Ang II) promotes inflammation and the generation of reactive oxygen species and governs onset and progression of vascular senescence, which are all associated with functional and structural changes, contributing to age-related diseases. Although the vast majority of the actions of Ang II, including vascular senescence, are mediated by the Ang II type 1 receptor (AT1R), the identification, characterization, and cloning of the angiotensin type 2 receptor has focused attention on this receptor and to its antagonistic effect on the detrimental effects of AT1R. This review provides an overview of the changes in RAS with aging and age-disease interactions culminating in the development of frailty.
在过去的几十年中，人们对肾素-血管紧张素系统（RAS）的认识有了显著的提高。现在认为，RAS 在几乎每个器官系统的生理和病理生理机制中都起着关键作用，是高血压、心血管疾病和肾功能的关键调节剂。血管紧张素 II（Ang II）促进炎症和活性氧的产生，并控制血管衰老的发生和进展，所有这些都与功能和结构变化有关，导致与年龄相关的疾病。尽管 Ang II 的绝大多数作用，包括血管衰老，都是通过 Ang II 型 1 受体（AT1R）介导的，但血管紧张素 2 型受体的鉴定、特征描述和克隆引起了人们对该受体的关注，并关注其对 AT1R 的有害作用的拮抗作用。这篇综述概述了 RAS 随年龄的变化以及年龄与疾病的相互作用，最终导致衰弱的发生。
