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dc.creatorTriposkiadis F., Starling R.C., Xanthopoulos A., Butler J., Boudoulas H.en
dc.date.accessioned2023-01-31T10:10:18Z
dc.date.available2023-01-31T10:10:18Z
dc.date.issued2021
dc.identifier10.1007/s10741-020-10022-4
dc.identifier.issn13824147
dc.identifier.urihttp://hdl.handle.net/11615/79794
dc.description.abstractCoronavirus disease 2019 (COVID-19) is due to severe acute respiratory syndrome coronavirus (SARS-CoV)-2 which binds and enters the host cells through the angiotensin-converting enzyme (ACE)2. While the potential for benefit with the use of renin-angiotensin-aldosterone system inhibitors (RAASi) and the risks from stopping them is more evident, potential harm by RAΑSi may also be caused by the increase in the activity of the ACE2 receptor, the inefficient counter regulatory axis in the lungs in which the proinflammatory prolyloligopeptidase (POP) is the main enzyme responsible for the conversion of deleterious angiotensin (ANG) II to protective ANG [1–7] and the proinflammatory properties of ACE2(+) cells infected with SARS-CoV-2. Acknowledging the proven RAΑSi benefit in patients with several diseases such as hypertension, heart failure, coronary disease, and diabetic kidney disease in the non-COVID-19 era, it is a reasonable strategy in this period of uncertainty to use these agents judiciously with careful consideration and to avoid the use of RAASi in select patients whenever possible, until definitive evidence becomes available. © 2020, Springer Science+Business Media, LLC, part of Springer Nature.en
dc.language.isoenen
dc.sourceHeart Failure Reviewsen
dc.source.urihttps://www.scopus.com/inward/record.uri?eid=2-s2.0-85090219664&doi=10.1007%2fs10741-020-10022-4&partnerID=40&md5=66fd29b76916bc5b5f6791d4d2419655
dc.subjectaldosteroneen
dc.subjectangiotensin IIen
dc.subjectdipeptidyl carboxypeptidaseen
dc.subjectferritinen
dc.subjectinfluenza vaccineen
dc.subjectinterleukin 6en
dc.subjectsodium glucose cotransporter 2en
dc.subjecttroponinen
dc.subjecttroponin Ten
dc.subjectdipeptidyl carboxypeptidase inhibitoren
dc.subjectacute coronary syndromeen
dc.subjectblood pressure regulationen
dc.subjectcoronavirus disease 2019en
dc.subjectcytokine releaseen
dc.subjectenzyme activityen
dc.subjectforced vital capacityen
dc.subjectheart ejection fractionen
dc.subjectheart failureen
dc.subjectheart left ventricle ejection fractionen
dc.subjectheart ventricle remodelingen
dc.subjecthemodynamicsen
dc.subjecthormone substitutionen
dc.subjecthospitalizationen
dc.subjecthost cellen
dc.subjecthumanen
dc.subjecthypertensionen
dc.subjectimmune responseen
dc.subjectimmunohistochemistryen
dc.subjectnonhumanen
dc.subjectpandemicen
dc.subjectphysical activityen
dc.subjectprevalenceen
dc.subjectprotein expressionen
dc.subjectrenin angiotensin aldosterone systemen
dc.subjectReviewen
dc.subjectvirus entryen
dc.subjectdrug effecten
dc.subjectrenin angiotensin aldosterone systemen
dc.subjectAngiotensin-Converting Enzyme Inhibitorsen
dc.subjectCOVID-19en
dc.subjectHumansen
dc.subjectRenin-Angiotensin Systemen
dc.subjectSpringeren
dc.titleRenin-angiotensin-system inhibition in the context of corona virus disease-19: experimental evidence, observational studies, and clinical implicationsen
dc.typeotheren


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