Pathophysiological mechanisms of COVID-19-related endothelial dysfunction and potential therapies

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Pathophysiological mechanisms of COVID-19-related endothelial dysfunction and potential therapies
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Pathophysiological mechanisms of COVID-19-related endothelial dysfunction and potential therapies MDPIOpenAccess UMG_Tweet SARSCoV2 COVID19 EndothelialDysfunction

By Dr. Chinta SidharthanOct 19 2022Reviewed by Aimee Molineux In a recent review published in Life, researchers discussed the pathophysiological mechanisms of endothelial dysfunction associated with severe coronavirus disease 2019 . They commented on the potential therapeutic strategies to treat endothelial damage and coagulopathy related to COVID-19.

Endothelial dysfunction The review reported the possible mechanisms that explain the SARS-CoV-2 tropism towards endothelial cells. Viral entry into the host cell begins with the binding of the SARS-CoV-2 spike protein to the angiotensin-converting enzyme-2 receptor and downstream activation of the spike protein subunits. The ACE-2 enzyme modulates the renin-angiotensin-aldosterone system signaling pathway, which controls local and systemic blood flow and pressure.

Severe COVID-19 is associated with extremely elevated levels of interleukins such as IL-1β, IL-10, IL-6, and IL-7, also known as “cytokine storm,” which increases tumor necrosis factor secretion and interferon-γ induced apoptosis. The elevated cytokines cause endothelial damage, which further increases the secretion of inflammatory molecules, causing a cyclic reaction.

Extrapulmonary manifestations can be seen in multiple organ systems, including the cardiac, renal, nervous, and gastrointestinal systems. Complications include arrhythmias, myocarditis, proteinuria, kidney failure, seizures, encephalopathy, cerebrovascular disease, intestinal inflammations, deep vein thrombosis, and many more.

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