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Currently, the emergence of a novel human corona virus, SARS-CoV-2, has become a global health concern causing severe symptoms. Angiotensin-converting enzyme 2 (ACE2) was intensively studied in the early 2000's because it binds with the spike protein of corona viruses SARS-COV and HCoV-NL63. This interaction is mediated by the ras-binding domain (RBD) of the spike protein, and is believed to be the pivotal event in the membrane fusion process. Recently, ACE2 has come back to the spotlight amid the outbreak of another deadly coronavirus, SARS-COV-2 (formerly 2019-nCoV). ACE2 is an integral component of the renin-angiotensin system (RAS). It is highly expressed in the vasculature, the kidney, lungs, and heart where its actions on peptide signals balance and offset those of ACE. The loss of ACE2 appears far more important in the development and progression of some cardiovascular diseases (CVD). There is a noticed increase of some inflammatory mediators as Lactate dehydrogenase (LDH), ferritin and C-reactive protein (CRP) with low neutrophile count in patient with SARS-CoV-2(COVID-19). There is significantly different clinical features between COVID-19-caused and non-COVID-19-caused pneumonia, especially in term of lymphocytopenia and organ injury. Notably, correlation analysis demonstrates that tissue damage in COVID-19 patients is attributed to virus infection itself rather than uncontrolled inflammatory responses. We therefore shed the light on all available information about the treatment of the cases, especially critical cases to decrease the mortality rate and maintain some important mediators within their important limits to give a great chance for the body and immune system to counteracts and eradicates the virus without further complications by a symptomatic treatment of COVID-19. Among our suggestions are Ang-(1-7) and/or GLP-1 receptor agonists as will be discussed in this short communication.
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Elkabily et al. (2020) studied this question.
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