Department of Vascular Surgery, University Hospital Zürich, Zürich, Switzerland.
Department of Molecular Life Sciences, University of Zürich, Switzerland.
Clin Sci (Lond). 2022 Nov 11;136(21):1571-1590. doi: 10.1042/CS20220235.
Although COVID-19 is primarily a respiratory disease, it may affect also the cardiovascular system. COVID-19 patients with cardiovascular disorder (CVD) develop a more severe disease course with a significantly higher mortality rate than non-CVD patients. A common denominator of CVD is the dysfunction of endothelial cells (ECs), increased vascular permeability, endothelial-to-mesenchymal transition, coagulation, and inflammation. It has been assumed that clinical complications in COVID-19 patients suffering from CVD are caused by SARS-CoV-2 infection of ECs through the angiotensin-converting enzyme 2 (ACE2) receptor and the cellular transmembrane protease serine 2 (TMPRSS2) and the consequent dysfunction of the infected vascular cells. Meanwhile, other factors associated with SARS-CoV-2 entry into the host cells have been described, including disintegrin and metalloproteinase domain-containing protein 17 (ADAM17), the C-type lectin CD209L or heparan sulfate proteoglycans (HSPG). Here, we discuss the current data about the putative entry of SARS-CoV-2 into endothelial and smooth muscle cells. Furthermore, we highlight the potential role of long non-coding RNAs (lncRNAs) affecting vascular permeability in CVD, a process that might exacerbate disease in COVID-19 patients.
虽然 COVID-19 主要是一种呼吸道疾病，但它也可能影响心血管系统。患有心血管疾病 (CVD) 的 COVID-19 患者的疾病进程更为严重，死亡率明显高于非 CVD 患者。CVD 的一个共同特征是内皮细胞 (ECs) 功能障碍、血管通透性增加、内皮到间充质转化、凝血和炎症。人们假设，患有 CVD 的 COVID-19 患者的临床并发症是由 SARS-CoV-2 通过血管紧张素转换酶 2 (ACE2) 受体和细胞跨膜丝氨酸蛋白酶 2 (TMPRSS2) 感染 ECs 引起的，随后感染的血管细胞功能障碍。与此同时，已经描述了与 SARS-CoV-2 进入宿主细胞相关的其他因素，包括解整合素和金属蛋白酶域蛋白 17 (ADAM17)、C 型凝集素 CD209L 或硫酸乙酰肝素蛋白聚糖 (HSPG)。在这里，我们讨论了关于 SARS-CoV-2 进入内皮细胞和平滑肌细胞的现有数据。此外，我们强调了长链非编码 RNA (lncRNA) 在 CVD 中影响血管通透性的潜在作用，这一过程可能会使 COVID-19 患者的病情恶化。
