Abstract

Coronavirus disease 2019 (COVID-19) can occur due to contracting severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). COVID-19 has no confined treatment and, consequently, has high hospitalization and mortality rates. Moreover, people who contract COVID-19 present systemic inflammatory spillover. It is now known that COVID-19 pathogenesis is linked to the renin-angiotensin system (RAS). COVID-19 invades host cells via the angiotensin-converting enzyme 2 (ACE2) receptor—as such, an individual's susceptibility to COVID-19 increases alongside the upregulation of this receptor. COVID-19 has also been associated with interstitial pulmonary fibrosis, which leads to acute respiratory distress, cardiomyopathy, and shock. These outcomes are thought to result from imbalances in angiotensin (Ang) II and Ang-(1-7)/alamandine activity. ACE2, Ang-(1-7), and alamandine have potent anti-inflammatory properties, and some SARS-CoV-2 patients exhibit high levels of ACE2 and Ang-(1-7). This phenomenon could indicate a failing physiological response to prevent or reduce the severity of inflammation-mediated pulmonary injuries. Alamandine, which is another protective component of the RAS, has several health benefits owing to its antithrombogenic, anti-inflammatory, and antifibrotic characteristics. Alamandine alleviates pulmonary fibrosis via the Mas-related G protein-coupled receptor D (MrgD). Thus, a better understanding of this pathway could uncover novel pharmacological strategies for altering proinflammatory environments within the body. Following such strategies could inhibit fibrosis after SARS-CoV-2 infection and, consequently, prevent COVID-19.

Highlights

  • COVID-19 is an extremely contagious disease triggered by severe acute respiratory syndrome coronavirus 2 (SARSCoV-2)

  • Coronaviruses comprise a single-stranded RNA enveloped in a capsid that is encapsulated in a spike (S) glycoprotein containing membrane

  • The angiotensin-converting enzyme 2 (ACE2)/Ang-(1-7)/mitochondrial assembly receptor (MasR) and alamandine/Mas-related G protein-coupled receptor D (MrgD) axes might help protect the body against COVID-19 [29] (Figure 1)

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Summary

Introduction

COVID-19 is an extremely contagious disease triggered by severe acute respiratory syndrome coronavirus 2 (SARSCoV-2). According to Zhou et al, SARS-CoV-2 can infiltrate ACE2-expressing cells, whereas it cannot enter cells that do not have ACE2 It cannot enter cells with conventional COVID-19 entry receptors such as aminopeptidase N and dipeptidyl peptidase 4 (DPP4) [6]. Such findings signify ACE2’s status as the primary cell receptor for SARS-CoV-2 [7]. We discuss the following: (i) different treatment options for COVID-19 patients and some clinical strategies for rebalancing the RAS These treatments utilize ACE inhibitors and angiotensin receptor blockers, and they involve the activation of the RAS’s protective arm with MasR agonist (Ang-(1-7)), (ii) ACE2-based treatments, and (iii) the protective effect of alamandine on COVID-19 patients, because of its anti-inflammatory, antifibrotic, and antioxidative properties. The search terms were alamandine, RAS, ACE2, Ang-(1-7), COVID-19, SARS-CoV-2, and cytokine storm; we searched for combinations of these terms

Treatments for COVID-19
The Renin-Angiotensin System
The Protective Arm of RAS
Angiotensin-Converting Enzyme 2
Angiotensin 1-7
Recruiting
Alamandine
Findings
Conclusion
Full Text
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