clearly determined that the S protein binds to CD147 in human cardiac pericytes. Even though ACE2 appears to be the primary receptor that binds the S protein of SARS-CoV-2 to cause infection, there is evidence that CD147, neuropilin-1, dipeptidyl peptidase 4, alanyl aminopeptidase, and glutamyl aminopeptidase can act as receptors for the S protein. Several receptors have been implicated in SAR-CoV-2 infection and S protein actions in COVID-19 patients. These findings clearly implicate the S protein as mediating cellular dysfunction however, the receptors and signaling mechanisms vary depending on the cell type. Human epithelial cells demonstrated increased senescence and inflammation following transfection with the S protein. Other actions of the S protein include direct stimulation of peripheral nerves, release of inflammatory factors, and stimulation of vasoactive mediators such as platelet-activating factor (PAF). A previous study demonstrated that the S protein could damage the endothelium and disrupt the blood–brain ba. The concept that the S protein can cause detrimental effects in COVID-19 patients independent of infection could partially explain the long-term health issues. Taken together, COVID-19 studies demonstrate that SAR-CoV-2 infection via ACE2 and the circulating S protein independent of infection can lead to cardiovascular dysfunction. It was further demonstrated that the S protein was capable of increasing cardiac pericyte migration, reduced endothelial cell network formation in Matrigel, induced pericyte cytokine secretion, and increased production of pro-apoptotic factors leading to endothelial cell death. Findings in this study determined that close to 70% of the patients did not have their pericytes infected by SARS-CoV-2. demonstrated the presence of the SARS-CoV-2 S protein in the peripheral blood of COVID-19 patients. The cytokine storm and hypoxia-induced actions leading to cardiomyocyte apoptosis is another mechanism suggested for cardiovascular mortality in COVID-19 patients. A potential mechanism for cardiac disease in COVID-19 has been myocardial involvement mediated by ACE2. The mechanisms by which COVID-19 causes or enhances cardiovascular diseases have been under intense investigation. Cardiovascular disorders such as myocardial infarction, arrhythmias, and thromboembolism appear to be a consequence of COVID-19. As such, the long-term consequences of SARS-CoV-2 on multiple organ systems needs to be evaluated. We have reached the 2-year anniversary for the COVID-19 pandemic, and it is clear that SARS-CoV-2 will become an endemic virus. Thus, blocking the CD147 receptor in COVID-19 patients could decrease cardiovascular disease caused by the circulating S protein. determined that the S protein actions on the cardiac pericytes are through cluster of differentiation 147 (CD147)-receptor mediated signaling. Cardiac pericytes are mural cells that support the maintenance and repair of the vasculature in the heart. in this edition of Clinical Science found that circulating SARS-CoV-2 spike (S) protein in the circulation can cause detrimental effects on cardiac pericytes independent of viral infection. The increase in cardiovascular events in COVID-19 patients has been widely thought to be mediated by infection by SARS-CoV-2 and uptake by angiotensin-converting enzyme-2 (ACE2). Future studies are needed to determine the effect of the S protein on pericytes in other organs and evaluate the effectiveness of CD147 receptor-blocking therapies to decrease organ damage caused by the S protein.ĬOVID-19 has been determined to increase mortality in patients with underlying cardiovascular conditions. These findings support the notion that circulating SARS-CoV-2 S protein could contribute to cardiovascular disease independent of viral infection. previously determined that the S protein acting through the cluster of differentiation 147 (CD147) receptor, and another unknown mechanism had detrimental effects on human cardiac pericytes ( Clin Sci (Lond) (2021) 135 (24): 2667–2689. Experimental findings are demonstrating that the circulating S protein can bind to receptors resulting in inflammation and cell, tissue, and organ damage. Interestingly, the SARS-CoV-2 spike (S) protein can be found circulating in the blood of COVID-19 patients. The SARS-CoV-2 virus that results in COVID-19 has been found to damage multiple organs beyond the lung.
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