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.

本综述重点关注衰老通过雌激素代谢、氧化应激和炎症的改变对流动介导的外向重塑 (FMR) 的影响。在缺血性疾病中，血管系统适应或重塑的能力决定了恢复的质量。FMR 在血运重建中起关键作用，是一种复杂的现象，可以招募内皮细胞和平滑肌细胞以及免疫系统。由于炎症和氧化应激的增加，部分线粒体起源，FMR 会随着年龄的增长而逐渐减少。FMR 的改变在有危险因素的老年人中更大，因此治疗不能仅仅等同于有或没有温和血管舒张药物的运动。有趣的是，女性 FMR 的降低发生得更晚。雌激素及其 α 受体 (ERα) 通过控制包括血管紧张素 II 2 型受体在内的扩张通路在 FMR 中发挥关键作用，从而为激活老年受试者的 FMR 提供了可能的工具，尽管只有实验数据可用。事实上，主要问题是随着时间的推移引起的血管损伤的可逆性，迄今为止，促进预防和限制暴露于风险因素仍然是这方面的最佳选择。