Relationship Between ACE2 and Other Components of the Renin-Angiotensin System.
Identifieur interne : 000099 ( Main/Corpus ); précédent : 000098; suivant : 000100Relationship Between ACE2 and Other Components of the Renin-Angiotensin System.
Auteurs : Jordana B. Cohen ; Thomas C. Hanff ; Adam P. Bress ; Andrew M. SouthSource :
- Current hypertension reports [ 1534-3111 ] ; 2020.
English descriptors
- KwdEn :
- MESH :
- chemical , physiology : Peptidyl-Dipeptidase A, Receptors, Virus.
- physiopathology : Coronavirus Infections, Pneumonia, Viral.
- Betacoronavirus, Humans, Pandemics, Renin-Angiotensin System.
Abstract
PURPOSE OF THE REVIEW
Angiotensin-converting enzyme 2 (ACE2) is a key counter-regulatory component of the renin-angiotensin system. Here, we briefly review the mechanistic and target organ effects related to ACE2 activity, and the importance of ACE2 in SARS-CoV-2 infection.
RECENT FINDINGS
ACE2 converts angiotensin (Ang) II to Ang-(1-7), which directly opposes the vasoconstrictive, proinflammatory, and prothrombotic effects of Ang II. ACE2 also facilitates SARS-CoV-2 viral entry into host cells. Drugs that interact with the renin-angiotensin system may impact ACE2 expression and COVID-19 pathogenesis; however, the magnitude and direction of these effects are unknown at this time. High quality research is needed to improve our understanding of how agents that act on the renin-angiotensin system impact ACE2 and COVID-19-related disease outcomes.
DOI: 10.1007/s11906-020-01048-y
PubMed: 32591908
PubMed Central: PMC7317893
Links to Exploration step
pubmed:32591908Le document en format XML
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Hanff</name><affiliation><nlm:affiliation>Department of Biostatistics, Epidemiology, and Informatics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA.</nlm:affiliation></affiliation><affiliation><nlm:affiliation>Division of Cardiology, Department of Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Bress, Adam P" sort="Bress, Adam P" uniqKey="Bress A" first="Adam P" last="Bress">Adam P. Bress</name><affiliation><nlm:affiliation>Division of Health System Innovation and Research, Department of Population Health Sciences, University of Utah, Salt Lake City, UT, USA.</nlm:affiliation></affiliation></author><author><name sortKey="South, Andrew M" sort="South, Andrew M" uniqKey="South A" first="Andrew M" last="South">Andrew M. South</name><affiliation><nlm:affiliation>Section of Nephrology, Department of Pediatrics, Wake Forest School of Medicine and Brenner Children's Hospital, Winston Salem, USA.</nlm:affiliation></affiliation><affiliation><nlm:affiliation>Department of Epidemiology and Prevention, Division of Public Health Sciences, Wake Forest School of Medicine, Winston Salem, USA.</nlm:affiliation></affiliation><affiliation><nlm:affiliation>Department of Surgery-Hypertension and Vascular Research, Wake Forest School of Medicine, Winston Salem, NC, USA.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2020">2020</date><idno type="RBID">pubmed:32591908</idno><idno type="pmid">32591908</idno><idno type="doi">10.1007/s11906-020-01048-y</idno><idno type="pmc">PMC7317893</idno><idno type="wicri:Area/Main/Corpus">000099</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">000099</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Relationship Between ACE2 and Other Components of the Renin-Angiotensin System.</title><author><name sortKey="Cohen, Jordana B" sort="Cohen, Jordana B" uniqKey="Cohen J" first="Jordana B" last="Cohen">Jordana B. Cohen</name><affiliation><nlm:affiliation>Renal-Electrolyte and Hypertension Division, Department of Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA. jco@pennmedicine.upenn.edu.</nlm:affiliation></affiliation><affiliation><nlm:affiliation>Department of Biostatistics, Epidemiology, and Informatics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA. jco@pennmedicine.upenn.edu.</nlm:affiliation></affiliation></author><author><name sortKey="Hanff, Thomas C" sort="Hanff, Thomas C" uniqKey="Hanff T" first="Thomas C" last="Hanff">Thomas C. Hanff</name><affiliation><nlm:affiliation>Department of Biostatistics, Epidemiology, and Informatics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA.</nlm:affiliation></affiliation><affiliation><nlm:affiliation>Division of Cardiology, Department of Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Bress, Adam P" sort="Bress, Adam P" uniqKey="Bress A" first="Adam P" last="Bress">Adam P. Bress</name><affiliation><nlm:affiliation>Division of Health System Innovation and Research, Department of Population Health Sciences, University of Utah, Salt Lake City, UT, USA.</nlm:affiliation></affiliation></author><author><name sortKey="South, Andrew M" sort="South, Andrew M" uniqKey="South A" first="Andrew M" last="South">Andrew M. South</name><affiliation><nlm:affiliation>Section of Nephrology, Department of Pediatrics, Wake Forest School of Medicine and Brenner Children's Hospital, Winston Salem, USA.</nlm:affiliation></affiliation><affiliation><nlm:affiliation>Department of Epidemiology and Prevention, Division of Public Health Sciences, Wake Forest School of Medicine, Winston Salem, USA.</nlm:affiliation></affiliation><affiliation><nlm:affiliation>Department of Surgery-Hypertension and Vascular Research, Wake Forest School of Medicine, Winston Salem, NC, USA.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Current hypertension reports</title><idno type="eISSN">1534-3111</idno><imprint><date when="2020" type="published">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Betacoronavirus (MeSH)</term><term>Coronavirus Infections (physiopathology)</term><term>Humans (MeSH)</term><term>Pandemics (MeSH)</term><term>Peptidyl-Dipeptidase A (physiology)</term><term>Pneumonia, Viral (physiopathology)</term><term>Receptors, Virus (physiology)</term><term>Renin-Angiotensin System (MeSH)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Peptidyl-Dipeptidase A</term><term>Receptors, Virus</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Coronavirus Infections</term><term>Pneumonia, Viral</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Betacoronavirus</term><term>Humans</term><term>Pandemics</term><term>Renin-Angiotensin System</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p><b>PURPOSE OF THE REVIEW</b></p><p>Angiotensin-converting enzyme 2 (ACE2) is a key counter-regulatory component of the renin-angiotensin system. Here, we briefly review the mechanistic and target organ effects related to ACE2 activity, and the importance of ACE2 in SARS-CoV-2 infection.</p></div><div type="abstract" xml:lang="en"><p><b>RECENT FINDINGS</b></p><p>ACE2 converts angiotensin (Ang) II to Ang-(1-7), which directly opposes the vasoconstrictive, proinflammatory, and prothrombotic effects of Ang II. ACE2 also facilitates SARS-CoV-2 viral entry into host cells. Drugs that interact with the renin-angiotensin system may impact ACE2 expression and COVID-19 pathogenesis; however, the magnitude and direction of these effects are unknown at this time. High quality research is needed to improve our understanding of how agents that act on the renin-angiotensin system impact ACE2 and COVID-19-related disease outcomes.</p></div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" IndexingMethod="Curated" Owner="NLM"><PMID Version="1">32591908</PMID><DateCompleted><Year>2020</Year><Month>07</Month><Day>08</Day></DateCompleted><DateRevised><Year>2020</Year><Month>07</Month><Day>21</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1534-3111</ISSN><JournalIssue CitedMedium="Internet"><Volume>22</Volume><Issue>7</Issue><PubDate><Year>2020</Year><Month>06</Month><Day>26</Day></PubDate></JournalIssue><Title>Current hypertension reports</Title><ISOAbbreviation>Curr. Hypertens. Rep.</ISOAbbreviation></Journal><ArticleTitle>Relationship Between ACE2 and Other Components of the Renin-Angiotensin System.</ArticleTitle><Pagination><MedlinePgn>44</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1007/s11906-020-01048-y</ELocationID><Abstract><AbstractText Label="PURPOSE OF THE REVIEW">Angiotensin-converting enzyme 2 (ACE2) is a key counter-regulatory component of the renin-angiotensin system. Here, we briefly review the mechanistic and target organ effects related to ACE2 activity, and the importance of ACE2 in SARS-CoV-2 infection.</AbstractText><AbstractText Label="RECENT FINDINGS">ACE2 converts angiotensin (Ang) II to Ang-(1-7), which directly opposes the vasoconstrictive, proinflammatory, and prothrombotic effects of Ang II. ACE2 also facilitates SARS-CoV-2 viral entry into host cells. Drugs that interact with the renin-angiotensin system may impact ACE2 expression and COVID-19 pathogenesis; however, the magnitude and direction of these effects are unknown at this time. High quality research is needed to improve our understanding of how agents that act on the renin-angiotensin system impact ACE2 and COVID-19-related disease outcomes.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Cohen</LastName><ForeName>Jordana B</ForeName><Initials>JB</Initials><AffiliationInfo><Affiliation>Renal-Electrolyte and Hypertension Division, Department of Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA. jco@pennmedicine.upenn.edu.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Biostatistics, Epidemiology, and Informatics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA. jco@pennmedicine.upenn.edu.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hanff</LastName><ForeName>Thomas C</ForeName><Initials>TC</Initials><AffiliationInfo><Affiliation>Department of Biostatistics, Epidemiology, and Informatics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Division of Cardiology, Department of Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bress</LastName><ForeName>Adam P</ForeName><Initials>AP</Initials><AffiliationInfo><Affiliation>Division of Health System Innovation and Research, Department of Population Health Sciences, University of Utah, Salt Lake City, UT, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>South</LastName><ForeName>Andrew M</ForeName><Initials>AM</Initials><AffiliationInfo><Affiliation>Section of Nephrology, Department of Pediatrics, Wake Forest School of Medicine and Brenner Children's Hospital, Winston Salem, USA.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Epidemiology and Prevention, Division of Public Health Sciences, Wake Forest School of Medicine, Winston Salem, USA.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Surgery-Hypertension and Vascular Research, Wake Forest School of Medicine, Winston Salem, NC, USA.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>T32 HL007891</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>K23 HL133843</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 HL146818</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>K01 HL133468</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>UC4 DK108173</GrantID><Acronym>DK</Acronym><Agency>NIDDK NIH HHS</Agency><Country>United 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