Endothelial dysfunction in COVID-19: Current findings and therapeutic implications.

Endothelial dysfunction in COVID-19: Current findings and therapeutic implications.
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DOI:
10.1016/j.atherosclerosis.2020.10.014
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发表时间:
2020-12
期刊:
影响因子:
5.3
通讯作者:
Flammer AJ
Flammer AJ
中科院分区:
医学2区
文献类型:
--
作者:
Nägele MP;Haubner B;Tanner FC;Ruschitzka F;Flammer AJ

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2019冠状病毒病(COVID-19)增加了几种非肺部并发症的风险,如急性心肌损伤、肾衰竭或血栓栓塞事件。对这些现象的一个可能的统一解释可能是存在严重的内皮功能障碍和损伤。本文综述了内皮功能障碍与COVID-19的关系及其治疗意义。内皮功能障碍是增加严重COVID-19风险的关键合并症的常见特征,如高血压、肥胖、糖尿病、冠状动脉疾病或心力衰竭。初步研究表明,血管内皮细胞可被严重急性呼吸综合征冠状病毒2(SARS-CoV-2)感染,在COVID-19晚期病例中发现了广泛的内皮损伤和炎症证据。先前的证据已经确定了内皮细胞在维持和调节血管稳态和血液凝固中的关键作用。因此,COVID-19中内皮功能障碍的加重可能会损害器官灌注,并导致促凝状态,从而导致大血管和微血管血栓形成事件。已知血管紧张素转换酶(ACE)抑制剂、血管紧张素受体阻滞剂(ARB)和他汀类药物可改善内皮功能障碍。来自小型观察性研究和其他病毒感染的数据表明,COVID-19可能具有有益效果。目前正在研究的COVID-19的其他治疗方法也可能通过改善患者的内皮功能障碍来发挥作用。将治疗重点放在预防和改善内皮功能障碍上可以改善COVID-19的结局。目前正在进行几项临床试验来探索这一概念。新的证据表明内皮功能障碍与COVID-19的病理生理学有关。它可以解释并发症,如多器官损伤或血栓形成事件。有针对性的干预措施,如RAS抑制剂或他汀类药物可能会改善结果。在COVID-19中,影响内皮功能障碍的干预措施的研究正在进行中。
Coronavirus disease 2019 (COVID-19) increases the risk of several non-pulmonary complications such as acute myocardial injury, renal failure or thromboembolic events. A possible unifying explanation for these phenomena may be the presence of profound endothelial dysfunction and injury. This review provides an overview on the association of endothelial dysfunction with COVID-19 and its therapeutic implications. Endothelial dysfunction is a common feature of the key comorbidities that increase risk for severe COVID-19 such as hypertension, obesity, diabetes mellitus, coronary artery disease or heart failure. Preliminary studies indicate that vascular endothelial cells can be infected by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), and evidence of widespread endothelial injury and inflammation is found in advanced cases of COVID-19. Prior evidence has established the crucial role of endothelial cells in maintaining and regulating vascular homeostasis and blood coagulation. Aggravation of endothelial dysfunction in COVID-19 may therefore impair organ perfusion and cause a procoagulatory state resulting in both macro- and microvascular thrombotic events. Angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs) and statins are known to improve endothelial dysfunction. Data from smaller observational studies and other viral infections suggests a possible beneficial effect in COVID-19. Other treatments that are currently under investigation for COVID-19 may also act by improving endothelial dysfunction in patients. Focusing therapies on preventing and improving endothelial dysfunction could improve outcomes in COVID-19. Several clinical trials are currently underway to explore this concept. New evidence implicates endothelial dysfunction in the pathophysiology of COVID-19. It may explain complications such as multi-organ damage or thrombotic events. Targeted interventions such as RAS inhibitors or statins may improve outcomes. Studies on interventions that affect endothelial dysfunction are underway in COVID-19.
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