Han T, Ma S, Sun C, Zhang H, Qu G, Chen Y, et al. Also, CD209L/L-SIGN was identified as another receptor for mediating SARS-CoV-2 entry into human cells which can also interacts with ACE2 to facilitate SARS-CoV-2 entry [21]. An official website of the United States government. However, several JAK/STAT inhibitors such as ruxolitinib, tofacitinib and baricitinib can suppress cytokine signaling cascade. 2021;142:106946. Reis G, Dos Santos Moreira-Silva EA, Silva DCM, Thabane L, Milagres AC, Ferreira TS, et al. Dupont A, Rauch A, Staessens S, Moussa M, Rosa M, Corseaux D, et al. ACE2 angiotensin-converting enzyme-2, ACEI angiotensin converting enzyme inhibitors, ARB angiotensin receptor blockers, BRD4i bromodomain-containing protein 4 inhibitors, JAK janus kinase, SGLT2i sodium-glucose cotransporter-2 inhibitors. Redox imbalance links COVID-19 and myalgic encephalomyelitis - PNAS Curative anticoagulation prevents endothelial lesion in COVID-19 patients. Pang J, Xu F, Aondio G, Li Y, Fumagalli A, Lu M, et al. The spatio-temporal release of VEGF-A and its effects on endothelial proliferation, migration and capillary-like tube formation warrant further study. Front Med. To obtain Breithaupt-Faloppa AC, Correia CJ, Prado CM, Stilhano RS, Ureshino RP, Moreira LFP. To this end, lactate production from glycolysis pathway serves as a useful biomarker of EC barrier dysfunction [106]. However, pre-treatment of ECs with losartan (belonging to ARB) and lisinopril (belonging to ACEI), fail to affect the susceptibility of hEC to SARS-CoV-2 infection [131]. Single-cell transcriptomic atlas of primate cardiopulmonary aging. 2021;8:648290. Yamaoka-Tojo M. Vascular endothelial glycocalyx damage in COVID-19. After that, STATs translocate into cell nucleus to orchestrate the expression of inflammatory cytokines, further instigating the cytokine storm feedback loop. In a single-center observational study, 82% of critically ill COVID-19 patients have significantly lower plasma level of vitamin C [154]. Mensah SA, Cheng MJ, Homayoni H, Plouffe BD, Coury AJ, Ebong EE. In these cardiovascular complications, endothelial dysfunction plays a fundamental role [27]. COVID-19 can manifest with myocardial injury (ischemic heart disease, arrhythmias and cardiomyopathies), arterial stiffness, liver injury and kidney injury [3]. Despite the observed benefits of HIVC, conflicting results have been reported in severe COVID-19 patients [159]. TCM has a well-documented safety profile in protecting against COVID-19 on the basis of standard care. 2021;2021:8671713. Joffre J, Rodriguez L, Matthay ZA, Lloyd E, Fields AT, Bainton RJ, et al. 2021;137:106829. However, conclusions need to be analyzed with caution due to small sample size [165]. Metformin represents the first-line therapy for T2DM [123]. Meyer K, Patra T, Vijayamahantesh, Ray R. SARS-CoV-2 spike protein induces paracrine senescence and leukocyte adhesion in endothelial cells. Angpt-2 angiopoietin-2, CCL2 chemokine (C-C motif) ligand 2, ECs endothelial cells, FMD flow-mediated dilation, HMWM high-molecular-weight multimers, IL-1 interleukin-1, IL-6 interleukin 6, PDGF-BB platelet-derived growth factor BB, s-Flt soluble fms-like tyrosine kinase, sICAM1 soluble ICAM1, sVCAM1 soluble VCAM1, sVE-cadherin soluble vascular endothelial cadherin, TF tissue factor, TNF- tumor necrosis factor, VEGF-A vascular endothelial growth factor A, vWF von Willebrand factor. Effectiveness of therapeutic heparin versus prophylactic heparin on death, mechanical ventilation, or intensive care unit admission in moderately ill patients with covid-19 admitted to hospital: RAPID randomised clinical trial. Cell. 17-Estradiol, a potential ally to alleviate SARS-CoV-2 infection. Front Cardiovasc Med. Here, we reviewed the potential mechanism of endothelial activation in COVID-19 by overviewing the most recent literature, with the aim to provide targeted therapies (Fig.
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