COVID-19 and the Renin-Angiotensin System

Malha, Line; Mueller, Franco B.; Pecker, Mark S.; Mann, Samuel J.; August, Phyllis; Feig, Peter U.

doi:10.1016/j.ekir.2020.03.024

Cited by 41 publications

(46 citation statements)

References 9 publications

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“…Further studies are needed to better understand renal involvement in severe COVID-19 cases, especially since some pathophysiological hypotheses suggest the possibility of kidney damages related to COVID-19 infection. [100][101][102][103] The current research provides evidence-based elements that can help clinicians in decision making when dealing with COVID-19 cases. Future studies should explore novel biomarkers, such as non-coding RNAs or proteomics, for disease progression and severity of COVID-19 and similar diseases in order to build powerful prediction tools.…”

Section: Biochemical Abnormalities In Severe Covid-19 Casesmentioning

confidence: 99%

A meta-analysis of potential biomarkers associated with severity of coronavirus disease 2019 (COVID-19)

et al. 2020

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Background: Prognostic factors for the Coronavirus disease 2019 (COVID1-9) are not well established. This study aimed to summarize the available data on the association between the severity of COVID-19 and common hematological, inflammatory and biochemical parameters. Methods: EMBASE, MEDLINE, Web of sciences were searched to identify all published studies providing relevant data. Random-effects meta-analysis was used to pool effect sizes. Results: The bibliographic search yielded 287 citations, 31 of which were finally retained. Meta-analysis of standardized mean difference (SMD) between severe and non-severe COVID-19 cases showed that CK-MB (SMD = 0.

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Section: Biochemical Abnormalities In Severe Covid-19 Casesmentioning

confidence: 99%

A meta-analysis of potential biomarkers associated with severity of coronavirus disease 2019 (COVID-19)

et al. 2020

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“…ACE2, another important enzyme of the renin-angiotensin system regulates the level of Ang-II by cleaving it into heptapeptide, Ang-1-7. Ang-1-7 mediates its effects through binding with the Mas receptor and counteracts the deleterious effects of ACE/Ang-II/ AT1 axis [21]. Thus, ACE and ACE2 regulate blood pressure homeostasis in the cardiovascular system by maintaining the balance between Ang-II and Ang-1-7.…”

Section: Interaction Of Sars-cov-2 With Renin-angiotensin Systemmentioning

confidence: 99%

An Assessment on Impact of COVID-19 Infection in a Gender Specific Manner

Agrawal

Das

Nathani

et al. 2020

Stem Cell Rev and Rep

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Coronavirus disease 2019 (COVID-19) is caused by novel coronavirus Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). It was first time reported in December 2019 in Wuhan, China and thereafter quickly spread across the globe. Till September 19, 2020, COVID-19 has spread to 216 countries and territories. Severe infection of SARS-CoV-2 cause extreme increase in inflammatory chemokines and cytokines that may lead to multi-organ damage and respiratory failure. Currently, no specific treatment and authorized vaccines are available for its treatment. Renin angiotensin system holds a promising role in human physiological system specifically in regulation of blood pressure and electrolyte and fluid balance. SARS-CoV-2 interacts with Renin angiotensin system by utilizing angiotensin-converting enzyme 2 (ACE2) as a receptor for its cellular entry. This interaction hampers the protective action of ACE2 in the cells and causes injuries to organs due to persistent angiotensin II (Ang-II) level. Patients with certain comorbidities like hypertension, diabetes, and cardiovascular disease are under the high risk of COVID-19 infection and mortality. Moreover, evidence obtained from several reports also suggests higher susceptibility of male patients for COVID-19 mortality and other acute viral infections compared to females. Analysis of severe acute respiratory syndrome coronavirus (SARS) and Middle East respiratory syndrome coronavirus (MERS) epidemiological data also indicate a gender-based preference in disease consequences. The current review addresses the possible mechanisms responsible for higher COVID-19 mortality among male patients. The major underlying aspects that was looked into includes smoking, genetic factors, and the impact of reproductive hormones on immune systems and inflammatory responses. Detailed investigations of this gender disparity could provide insight into the development of patient tailored therapeutic approach which would be helpful in improving the poor outcomes of COVID-19.

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“…Those in favor of uninterrupted administration of RAS inhibitors would argue that, as illustrated in Figure 1C , depleting Ang II or blocking its action on AT1R [by ACE inhibitors or Ang-receptor blockers (ARBs), respectively] would balance the exhaustion of Ang 1-7 caused by viral invasion and might prevent consequent vasoconstriction ( South et al, 2020 ). Furthermore, it is also likely that the profile of Ang derivatives may differ in patients treated by ARBs, by ACE inhibitors or by spironolactone ( Malha et al, 2020 ). That is why blanket reassurance regarding continuation of RAS inhibitors during the current pandemic ( Vaduganathan et al, 2020 ) should be regarded with caution.…”

Section: Knowledge Gaps: the Missing Pieces In The Puzzlementioning

confidence: 99%

ACE2, COVID-19 Infection, Inflammation, and Coagulopathy: Missing Pieces in the Puzzle

et al. 2020

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Engulfed by the grave consequences of the coronavirus disease 2019 (COVID-19) pandemic, a better understanding of the unique pattern of viral invasion and virulence is of utmost importance. Angiotensin (Ang)-converting enzyme (ACE) 2 is a key component in COVID-19 infection. Expressed on cell membranes in target pulmonary and intestinal host cells, ACE2 serves as an anchor for initial viral homing, binding to COVID-19 spike-protein domains to enable viral entry into cells and subsequent replication. Viral attachment is facilitated by a multiplicity of membranal and circulating proteases that further uncover attachment loci. Inherent or acquired enhancement of membrane ACE2 expression, likely leads to a higher degree of infection and may explain the predisposition to severe disease among males, diabetics, or patients with respiratory or cardiac diseases. Additionally, once attached, viral intracellular translocation and replication leads to depletion of membranal ACE2 through degradation and shedding. ACE2 generates Ang 1-7, which serves a critical role in counterbalancing the vasoconstrictive, pro-inflammatory, and pro-coagulant effects of ACE-induced Ang II. Therefore, Ang 1-7 may decline in tissues infected by COVID-19, leading to unopposed deleterious outcomes of Ang II. This likely leads to microcirculatory derangement with endothelial damage, profound inflammation, and coagulopathy that characterize the more severe clinical manifestations of COVID-19 infection. Our understanding of COVID-ACE2 associations is incomplete, and some conceptual formulations are currently speculative, leading to controversies over issues such as the usage of ACE inhibitors or Ang-receptor blockers (ARBs). This highlights the importance of focusing on ACE2 physiology in the evaluation and management of COVID-19 disease.

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COVID-19 and the Renin-Angiotensin System

Cited by 41 publications

References 9 publications

A meta-analysis of potential biomarkers associated with severity of coronavirus disease 2019 (COVID-19)

A meta-analysis of potential biomarkers associated with severity of coronavirus disease 2019 (COVID-19)

An Assessment on Impact of COVID-19 Infection in a Gender Specific Manner

ACE2, COVID-19 Infection, Inflammation, and Coagulopathy: Missing Pieces in the Puzzle

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