In a recent review published in Life, researchers discussed the pathophysiological mechanisms of endothelial disorder relevant to severe coronavirus disease 2019 (COVID-19). They commented on possible cure to treat endothelial injury and COVID-19-like coagulopathy.
New studies show that while severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection primarily affects the pulmonary and respiratory systems, long-term fitness disorders related to microthromboembolism, myocardial injury, myocarditis, and renal failure have been observed in COVID-19 patients. A developing evidence framework indicates that endothelial damage due to viral infection and the COVID-19 inflammatory reaction would possibly be contributing to the severity of the disease.
Endothelial cells regulate inflammation, clotting, blood vessel dilation, and oxidative stress. Studies have shown that vascular endothelial damage and disorder contribute particularly to severe lung outcomes from COVID-19. In addition, many extrapulmonary symptoms of COVID-19 have also been linked to endothelial disorder. Exploring the pathophysiology of endothelial injury and reading possible treatment strategies can help limit the serious consequences of COVID-19.
The review reported on the conceivable mechanisms that explain the tropism of SARS-CoV-2 towards endothelial mobiles. 2) and downstream activation of spike protein subunits. The ACE-2 enzyme modulates the renin-angiotensin-aldosterone (RAAS) signaling pathway, which controls local and systemic blood flow and pressure.
The interactions of the spike protein with the κB nuclear pathway and integrin α5β1 are ideal for causing endothelial damage. SARS-CoV-2 is also ideal for adjusting endothelial glycoclelial integrity and endothelial cell apoptosis.
The authors also looked at inflammation and hypercoagulability resulting from endothelial damage. Endothelial cells produce endogenous molecules such as prostaglandin and nitric oxide that are responsible for controlling platelet aggregation and maintaining vascular homeostasis. Endothelial damage induces hypercoagulation and contractions of the vascular system, leading to an increased threat of thromboembolic events. Hypercoagulation also reduces blood to other areas, such as the kidneys and myocardium, leading to disseminated intravascular clotting.
Severe COVID-19 is linked to incredibly high levels of interleukins (IL) such as IL-1β, IL-10, IL-6, and IL-7, also known as a “cytokine storm,” which accumulates tumor necrosis secretion. and interferon-induced apoptosis-γ. High cytokines cause endothelial damage, which increases the secretion of inflammatory molecules, causing a cyclic reaction.
The review investigated studies comparing transmission, virulence and immune evasion of fear variants in SARS-CoV-2. The effects indicated that while the Omicron variant had mutations in the spike protein and obligate receptor domain that resulted in immune evasion and superior gearbox, it caused a decrease in severity and did not affect endothelial cells as much as the delta variant. Studies have found fewer incidences of pulmonary embolism related to the Omicron variant.
Pulmonary manifestations range from mild to severe and vary by comorbidities, age, sex, viral load, genetics, and ethnicity. Symptoms range from upper respiratory tract infections to hypoxia, acute respiratory distress syndrome, and pulmonary edema.
Extrapulmonary manifestations can be observed in various organ systems, adding the cardiac, renal, nervous and gastrointestinal systems. Complications come with arrhythmias, myocarditis, proteinuria, kidney failure, seizures, encephalopathy, cerebrovascular disease, intestinal inflammation, deep vein thrombosis, and many others.
Emerging in “long COVID” has revealed that endothelial damage is one of the points that contribute to chronic systemic disorders such as thrombosis, fatigue, heart headaches such as myocardial hypertrophy, and neurodegenerative symptoms experienced by COVID-19 patients in the months following their recovery.
Clinical trial data recommend various treatment methods to target coagulopathy and endothelial damage caused by COVID-19. Low molecular weight heparin exhibits antiviral and anti-inflammatory activity in addition to its antithrombotic effects. Corticosteroids are regularly used to treat respiratory symptoms of SARS-CoV-2 infections. In addition, corticosteroids exhibit anti-inflammatory activity and decrease procoagulation sites such as fibrinogen and von Willebrand factor.
Although debatable due to their role in expanding ACE-2 receptor expression and possibly facilitating viral entry, RAAS inhibitors are also thought to reduce endothelial damage. antibodies in the remedy of endothelial disorder and hypercoagulation.
To summarize, the review discussed the conceivable pathophysiological mechanisms of endothelial disorder affecting severe COVID-19 and causing immediate and long-term multi-organ damage. Endothelial disorder manifests primarily through hypercoagulation and inflammation, and the extent of endothelial damage varies depending on the SARS-CoV-2 variant of interest.
The authors presented knowledge from clinical trials on the use of heparins, RAAS inhibitors, corticosteroids, monoclonal antibodies, and many other healing features that can potentially be used to decrease endothelial damage caused by severe SARS-CoV-2 infections.
Written By
Chinta Sidharthan is a Bangalore-based India. Su academic background is in evolutionary biology and genetics, and has extensive experience in clinical studies, teaching, clinical writing and herpetology. Chinta holds a PhD in evolutionary biology from the Indian Institute of Science and is passionate about science education, writing, animals, wildlife and conservation. For his doctoral studies, he explored the origins and diversification of blind snakes in India, where he conducted extensive fieldwork in the jungles of southern India. He has won the Governor General Bronze Medal and Gold Medal for Academic Excellence award from the University of Bangalore and has published his studies in high-impact journals.
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