Background: COVID-19 has continued to generate concerns from across the globe with symptoms ranging from mild to acute ones. The disease has been linked to angiotensin-converting enzyme (ACE) 1 and 2, but ACE1 has been lowly researched.
Aim: To conduct a systematic review that explores the role of Angiotensin-Converting Enzymes ACE1 and ACE 2 in COVID-19 Infection and the clinical conditions of the patients with the disease.
Materials and Methods: the guidelines of PRISMA were used to select 40 journal articles across various databases namely PubMed, Cochrane Central Register of Controlled Trials (CENTRAL), and Embase for researches between 2019 and 2021. Various key terms were employed in the search process, such as "Covid-19," "Covid," "Corona Virus," "ACE," "Angiotensin-Converting Enzyme," “SARS-CoV-2,” “ACE1,” “ACE2,” and “angiotensin receptors.” The search terms were combined using Boolean operators “and/or” incomplete sentences affiliated with the topic in order to generate substantial results.
Results: COVID-19 pathologies/severity are affiliated with inverse proportionality of ACE1/ACE2 ratio. High ACE2 levels in adults act as the targets for COVID-19 while in children the high level of ACE2 is not associated with the disease’s severity. ACE1 contributes to cytokine production, which contributes to ARDS.
Discussion: Imbalanced ratio of ACE1/ACE2 increase COVID-19 severity. However, the findings apply to patients with hypertension, and therefore, more research would be needed for other pathologies of COVID-19.
Conclusion: Both the ACE1 and ACE2 are affiliated with COVID-19 severity. Therefore, ACE1/ACE2 activities can be used as markers to reflect the clinical conditions of COVID-19, thereby helping to manage the disease efficiently.
Abstract
Background: COVID-19 has continued to generate concerns from across the globe with symptoms ranging from mild to acute ones. The disease has been linked to angiotensin-converting enzyme (ACE) 1 and 2, but ACE1 has been lowly researched.
Aim: To conduct a systematic review that explores the role of Angiotensin-Converting Enzymes ACE1 and ACE 2 in COVID-19 Infection and the clinical conditions of the patients with the disease.
Materials and Methods: the guidelines of PRISMA were used to select 40 journal articles across various databases namely PubMed, Cochrane Central Register of Controlled Trials (CENTRAL), and Embase for researches between 2019 and 2021. Various key terms were employed in the search process, such as "Covid-19," "Covid," "Corona Virus," "ACE," "Angiotensin-Converting Enzyme," “SARS-CoV-2,” “ACE1,” “ACE2,” and “angiotensin receptors.” The search terms were combined using Boolean operators “and/or” in complete sentences affiliated with the topic in order to generate substantial results.
Results: COVID-19 pathologies/severity are affiliated with inverse proportionality of ACE1/ACE2 ratio. High ACE2 levels in adults act as the targets for COVID-19 while in children the high level of ACE2 is not associated with the disease’s severity. ACE1 contributes to cytokine production, which contributes to ARDS.
Discussion: Imbalanced ratio of ACE1/ACE2 increase COVID-19 severity. However, the findings apply to patients with hypertension, and therefore, more research would be needed for other pathologies of COVID-19.
Conclusion: Both the ACE1 and ACE2 are affiliated with COVID-19 severity. Therefore, ACE1/ACE2 activities can be used as markers to reflect the clinical conditions of COVID-19, thereby helping to manage the disease efficiently.
Introduction
Since its inception in 2019, COVID-19 has produced a tremendous global health concern characterized by symptoms that range from mild to acute ones, such as respiratory failure, heart problems, acute respiratory distress syndrome (ARDS), and death [1–8]. The disease is caused by SARS-CoV-2 coronavirus [9]. Several studies have linked SARS-CoV-2 to angiotensin-converting enzyme 2 (ACE2) for host cell entry [10–12]. ACE2 is one of the axes that make up the renin-angiotensin system (RAS), which is responsible for maintaining blood pressure and balancing the electrolytes in the body. Particular scholars have associated RAS with ARDS pathogenesis [9]. The other axe component of RAS is ACE1, which is known for the deterioration of the respiratory system, while ACE2 works to protect the ARDS [9]. Being that ARDS is affiliated with COVID-19, then, determining the role played by RAS in the latter would be essential to aid in its management. Additionally, since ACE2 is the receptor of SARS-CoV-2, numerous researches have focused on it [13–15]. Currently, reports have been published indicating the clinical significance of ACE2 in treating COVID-19 patients [13]. Nonetheless. ACE1 has been lowly researched in relation to COVID-19 despite its significance in counterbalancing ACE2 in RAS.
ACE1 and ACE2 operate in a counter-regulatory relationship indicating that the elevated levels of one receptor are inversely proportional to the other [16,17]. ACE1 is localized on the endothelium’s luminal surface, and it is hyperactive in the endothelial cells of the lungs and also found in blood [9]. In the late 80s, ACE1 was reported as a biomarker to reflect on the severity of ARDS and damage of endothelial cells as triggered by other pathogens [9]. This implies that ACE1 can be perceived as a biomarker for the severity of COVID-19. Nonetheless, the inverse affiliations between ACE1 and ACE2 are still uncertain thereby sparking different discourses among scientific scholars.
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