Faculty of Medicine, 54694Vilnius University, Vilnius, Lithuania.
Department of Nephrology, Skåne University Hospital, Malmö, Sweden.
Angiology. 2023 Apr;74(4):308-316. doi: 10.1177/00033197221121007. Epub 2022 Aug 28.
Vascular age is determined by functional and structural changes in the arterial wall. When measured by its proxy, pulse wave velocity, it has been shown to predict cardiovascular and total mortality. Disconcordance between chronological and vascular age might represent better or worse vascular health. Cell senescence is caused by oxidative stress and sustained cell replication. Senescent cells acquire senescence-associated secretory phenotype. Oxidative stress, endothelial dysfunction, dysregulation of coagulation and leucocyte infiltration are observed in the aging endothelium. All of these mechanisms lead to increased vascular calcification and stiffness. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can involve the vascular endothelium. It enters cells using angiotensin-converting enzyme 2 (ACE-2) receptors, which are abundant in endothelial cells. The damage this virus does to the endothelium can be direct or indirect. Indirect damage is caused by hyperinflammation. Direct damage results from effects on ACE-2 receptors. The reduction of ACE-2 levels seen during coronavirus disease 2019 (COVID-19) infection might cause vasoconstriction and oxidative stress. COVID-19 and vascular aging share some pathways. Due to the novelty of the virus, there is an urgent need for studies that investigate its long-term effects on vascular health.
血管年龄取决于动脉壁的功能和结构变化。当通过其替代物脉搏波速度测量时，它已被证明可以预测心血管和全因死亡率。与实际年龄相比，血管年龄的不匹配可能代表血管健康状况更好或更差。细胞衰老由氧化应激和持续的细胞复制引起。衰老细胞获得衰老相关分泌表型。衰老内皮中观察到氧化应激、内皮功能障碍、凝血失调和白细胞浸润。所有这些机制都导致血管钙化和僵硬增加。严重急性呼吸综合征冠状病毒 2 (SARS-CoV-2) 可累及血管内皮。它使用血管紧张素转换酶 2 (ACE-2) 受体进入细胞，这些受体在血管内皮细胞中大量存在。该病毒对内皮的损害可以是直接的或间接的。间接损伤是由过度炎症引起的。直接损伤是由对 ACE-2 受体的影响引起的。在 2019 冠状病毒病 (COVID-19) 感染期间观察到的 ACE-2 水平降低可能导致血管收缩和氧化应激。COVID-19 和血管老化有一些共同的途径。由于该病毒的新颖性，迫切需要研究其对血管健康的长期影响。
