2020
DOI: 10.1053/j.jvca.2020.04.010
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The Renin-Angiotensin-Aldosterone System in Coronavirus Infection—Current Considerations During the Pandemic

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Cited by 7 publications
(7 citation statements)
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References 30 publications
(56 reference statements)
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“…The anchoring ability of the virus is due to its spike protein, which is present on its surface[ 71 , 147 , 148 ]. The dysregulation of RAAS occurs due to the loss of a counter-balance between Ang II levels and ACE2 levels after SARS-CoV-2 infection[ 149 ]. ACE2 levels degrade Ang II and produce Ang (1-7), which opposes the negative impact of Ang II[ 132 , 150 ].…”
Section: How Can the Interplay Between Dm And Covid-19 Increase The Rmentioning
confidence: 99%
“…The anchoring ability of the virus is due to its spike protein, which is present on its surface[ 71 , 147 , 148 ]. The dysregulation of RAAS occurs due to the loss of a counter-balance between Ang II levels and ACE2 levels after SARS-CoV-2 infection[ 149 ]. ACE2 levels degrade Ang II and produce Ang (1-7), which opposes the negative impact of Ang II[ 132 , 150 ].…”
Section: How Can the Interplay Between Dm And Covid-19 Increase The Rmentioning
confidence: 99%
“…4,5 Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) enters human cells by binding to the angiotensinconverting enzyme 2 (ACE-2) receptor. 6 This receptor is expressed in heart, lungs, kidneys, and intestines, thereby providing a multimodal entry point for the virus to infiltrate the body. Preliminary unpublished data indicate that ACE-2 receptor concentrations are higher in adipose tissue in comparison with lung tissue, suggesting that adipose tissue might be vulnerable to SARS-CoV-2 infection (preprint data available from https://www.preprints.org/manuscript/202002.0315/v1).…”
Section: Referencesmentioning
confidence: 99%
“…The first mechanism is that coronavirus can infect and directly destroy lymphocytes because they express the viral-binding protein on their surface membrane, namely angiotensin-converting enzyme 2. 19,20 A second mechanism for lymphopenia may be increased lymphocytic apoptosis due to the cytokine storm that may accompany infection with coronavirus. 7,21 This cytokine storm may also result in atrophy of lymphoid reserves, including the spleen, and impair lymphocyte levels.…”
Section: Consider the Complete Blood Countmentioning
confidence: 99%
“…The second observation is that thrombocytopenia may not always be present, suggesting alternative drivers for this thrombotic disorder, including viral endothelial damage and marked complement activation. 20,26,[31][32]36 Mechanisms beyond complement activation must also be considered for the thrombotic disorder in COVID-19. The elevated fibrinogen and factor VIII levels could also lead to thrombosis.…”
Section: Consider the Coagulation Systemmentioning
confidence: 99%