[Inhibitors of RAS Might Be a Good Choice for the Therapy of COVID-19 Pneumonia].
Identifieur interne : 000060 ( an2020/Analysis ); précédent : 000059; suivant : 000061[Inhibitors of RAS Might Be a Good Choice for the Therapy of COVID-19 Pneumonia].
Auteurs : M L Sun [République populaire de Chine] ; J M Yang [République populaire de Chine] ; Y P Sun [République populaire de Chine] ; G H Su [République populaire de Chine]Source :
- Zhonghua jie he he hu xi za zhi = Zhonghua jiehe he huxi zazhi = Chinese journal of tuberculosis and respiratory diseases [ 1001-0939 ] ; 2020.
Descripteurs français
- KwdFr :
- Angiotensine-II, Animaux, Fragments peptidiques, Humains, Infections à coronavirus (traitement médicamenteux), Inflammation (traitement médicamenteux), Inflammation (étiologie), Inhibiteurs de l'enzyme de conversion de l'angiotensine (usage thérapeutique), Peptidyl-Dipeptidase A (), Peptidyl-Dipeptidase A (physiologie), Pneumopathie virale (traitement médicamenteux), Pneumopathie virale (étiologie), Poumon, Pression sanguine (), Pronostic, Système rénine-angiotensine (), Système rénine-angiotensine (physiologie).
- MESH :
- physiologie : Peptidyl-Dipeptidase A, Système rénine-angiotensine.
- traitement médicamenteux : Infections à coronavirus, Inflammation, Pneumopathie virale.
- usage thérapeutique : Inhibiteurs de l'enzyme de conversion de l'angiotensine.
- étiologie : Inflammation, Pneumopathie virale.
- Angiotensine-II, Animaux, Fragments peptidiques, Humains, Peptidyl-Dipeptidase A, Poumon, Pression sanguine, Pronostic, Système rénine-angiotensine.
English descriptors
- KwdEn :
- Angiotensin II, Angiotensin-Converting Enzyme Inhibitors (therapeutic use), Animals, Betacoronavirus (drug effects), Betacoronavirus (pathogenicity), Blood Pressure (drug effects), Coronavirus Infections (drug therapy), Humans, Inflammation (drug therapy), Inflammation (etiology), Lung, Peptide Fragments, Peptidyl-Dipeptidase A (drug effects), Peptidyl-Dipeptidase A (physiology), Pneumonia, Viral (drug therapy), Pneumonia, Viral (etiology), Prognosis, Renin-Angiotensin System (drug effects), Renin-Angiotensin System (physiology).
- MESH :
- chemical , drug effects : Peptidyl-Dipeptidase A.
- chemical , physiology : Peptidyl-Dipeptidase A.
- chemical , therapeutic use : Angiotensin-Converting Enzyme Inhibitors.
- chemical : Angiotensin II, Peptide Fragments.
- drug effects : Betacoronavirus, Blood Pressure, Renin-Angiotensin System.
- drug therapy : Coronavirus Infections, Inflammation, Pneumonia, Viral.
- etiology : Inflammation, Pneumonia, Viral.
- pathogenicity : Betacoronavirus.
- physiology : Renin-Angiotensin System.
- Animals, Humans, Lung, Prognosis.
Abstract
The novel coronavirus 2019 (COVID-19) infected patients by binding human ACE2, leading to severe pneumonia and highly mortality rate in patients. At present, there is no definite and effective treatment for COVID-19. ACE2 plays an important role in the RAS, and the imbalance between ACE/Ang II/AT1R pathway and ACE2/Ang (1-7)/Mas receptor pathway in the RAS system will lead to multi-system inflammation. Increased ACE and Ang II are poor prognostic factors for severe pneumonia. Animal studies have shown that RAS inhibitors could effectively relieve symptoms of acute severe pneumonia and respiratory failure. The binding of COVID-19 and ACE2 resulted in the exhaustion of ACE2, and then ACE2/Ang (1-7)/Mas receptor pathway was inhibited. The balance of the RAS system was broken, and this would lead to the exacerbation of acute severe pneumonia. Therefore, we speculate that ACEI and AT1R inhibitors could be used in patients with COVID-19 pneumonia under the condition of controlling blood pressure, and might reduce the pulmonary inflammatory response and mortality.
DOI: 10.3760/cma.j.issn.1001-0939.2020.03.016
PubMed: 32164092
Affiliations:
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<front><div type="abstract" xml:lang="en">The novel coronavirus 2019 (COVID-19) infected patients by binding human ACE2, leading to severe pneumonia and highly mortality rate in patients. At present, there is no definite and effective treatment for COVID-19. ACE2 plays an important role in the RAS, and the imbalance between ACE/Ang II/AT1R pathway and ACE2/Ang (1-7)/Mas receptor pathway in the RAS system will lead to multi-system inflammation. Increased ACE and Ang II are poor prognostic factors for severe pneumonia. Animal studies have shown that RAS inhibitors could effectively relieve symptoms of acute severe pneumonia and respiratory failure. The binding of COVID-19 and ACE2 resulted in the exhaustion of ACE2, and then ACE2/Ang (1-7)/Mas receptor pathway was inhibited. The balance of the RAS system was broken, and this would lead to the exacerbation of acute severe pneumonia. Therefore, we speculate that ACEI and AT1R inhibitors could be used in patients with COVID-19 pneumonia under the condition of controlling blood pressure, and might reduce the pulmonary inflammatory response and mortality.</div>
</front>
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