MITOVASC Laboratory and CARFI Facility, INSERM U1083, CNRS UMR 6015, University of Angers, Angers, France.
MITOVASC Laboratory and CARFI Facility, INSERM U1083, CNRS UMR 6015, University of Angers, Angers, France.
Mech Ageing Dev. 2021 Mar;194:111416. doi: 10.1016/j.mad.2020.111416. Epub 2020 Dec 14.
The present review focuses on the effect of aging on flow-mediated outward remodeling (FMR) via alterations in estrogen metabolism, oxidative stress and inflammation. In ischemic disorders, the ability of the vasculature to adapt or remodel determines the quality of the recovery. FMR, which has a key role in revascularization, is a complex phenomenon that recruits endothelial and smooth muscle cells as well as the immune system. FMR becomes progressively less with age as a result of an increase in inflammation and oxidative stress, in part of mitochondrial origin. The alteration in FMR is greater in older individuals with risk factors and thus the therapy cannot merely amount to exercise with or without a mild vasodilating drug. Interestingly, the reduction in FMR occurs later in females. Estrogen and its alpha receptor (ERα) play a key role in FMR through the control of dilatory pathways including the angiotensin II type 2 receptor, thus providing possible tools to activate FMR in older subjects although only experimental data is available. Indeed, the main issue is the reversibility of the vascular damage induced over time, and to date promoting prevention and limiting exposure to the risk factors remain the best options in this regard.
本综述重点探讨了衰老通过改变雌激素代谢、氧化应激和炎症对血流介导的外向重塑（FMR）的影响。在缺血性疾病中，血管适应或重塑的能力决定了恢复的质量。FMR 在血管再通中起着关键作用，是一种涉及内皮细胞和平滑肌细胞以及免疫系统的复杂现象。随着年龄的增长，炎症和氧化应激的增加（部分源于线粒体），FMR 逐渐减少。有危险因素的老年人的 FMR 改变更大，因此治疗不仅仅是运动或使用温和的血管扩张药物。有趣的是，女性的 FMR 减少发生得更晚。雌激素及其α受体（ERα）通过控制包括血管紧张素 II 型 2 受体在内的扩张途径，在 FMR 中发挥关键作用，从而为在老年患者中激活 FMR 提供了可能的工具，尽管目前只有实验数据。事实上，主要问题是随着时间的推移诱导的血管损伤的可逆性，迄今为止，促进预防和限制暴露于危险因素仍然是这方面的最佳选择。
