[Inhibitors of RAS Might Be a Good Choice for the Therapy of COVID-19 Pneumonia].
Identifieur interne : 000054 ( PubMed/Checkpoint ); précédent : 000053; suivant : 000055[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.
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.1001-0939.2020.0014
PubMed: 32061198
Affiliations:
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Sciences, Department of Cardiology, Qilu Hospital of Shandong University, Jinan 250012, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese Ministry of Health and Chinese Academy of Medical Sciences, Department of Cardiology, Qilu Hospital of Shandong University, Jinan 250012</wicri:regionArea><wicri:noRegion> Jinan 250012</wicri:noRegion></affiliation></author><author><name sortKey="Sun, Y P" sort="Sun, Y P" uniqKey="Sun Y" first="Y P" last="Sun">Y P Sun</name><affiliation wicri:level="1"><nlm:affiliation>Department of Oncology, Jinan Central Hospital Affiliated to Shandong University, Jinan 250013, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Oncology, Jinan Central Hospital Affiliated to Shandong University, Jinan 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250013</wicri:noRegion></affiliation></author><author><name sortKey="Yang, J M" sort="Yang, J M" uniqKey="Yang J" first="J M" last="Yang">J M Yang</name><affiliation wicri:level="1"><nlm:affiliation>The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese Ministry of Health and Chinese Academy of Medical Sciences, Department of Cardiology, Qilu Hospital of Shandong University, Jinan 250012, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese Ministry of Health and Chinese Academy of Medical Sciences, Department of Cardiology, Qilu Hospital of Shandong University, Jinan 250012</wicri:regionArea><wicri:noRegion> Jinan 250012</wicri:noRegion></affiliation></author><author><name sortKey="Sun, Y P" sort="Sun, Y P" uniqKey="Sun Y" first="Y P" last="Sun">Y P Sun</name><affiliation wicri:level="1"><nlm:affiliation>Department of Oncology, Jinan Central Hospital Affiliated to Shandong University, Jinan 250013, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Oncology, Jinan Central Hospital Affiliated to Shandong University, Jinan 250013</wicri:regionArea><wicri:noRegion>Jinan 250013</wicri:noRegion></affiliation></author><author><name sortKey="Su, G H" sort="Su, G H" uniqKey="Su G" first="G H" last="Su">G H Su</name><affiliation wicri:level="1"><nlm:affiliation>Department of Cardiology, Jinan Central Hospital Affiliated to Shandong University, Jinan 250013, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Cardiology, Jinan Central Hospital Affiliated to Shandong University, Jinan 250013</wicri:regionArea><wicri:noRegion>Jinan 250013</wicri:noRegion></affiliation></author></analytic><series><title level="j">Zhonghua jie he he hu xi za zhi = Zhonghua jiehe he huxi zazhi = Chinese journal of tuberculosis and respiratory diseases</title><idno type="ISSN">1001-0939</idno><imprint><date when="2020" type="published">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><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></TEI><pubmed><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">32061198</PMID><DateRevised><Year>2020</Year><Month>02</Month><Day>15</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Print">1001-0939</ISSN><JournalIssue CitedMedium="Print"><Volume>43</Volume><Issue>0</Issue><PubDate><Year>2020</Year><Month>Feb</Month><Day>16</Day></PubDate></JournalIssue><Title>Zhonghua jie he he hu xi za zhi = Zhonghua jiehe he huxi zazhi = Chinese journal of tuberculosis and respiratory diseases</Title><ISOAbbreviation>Zhonghua Jie He He Hu Xi Za Zhi</ISOAbbreviation></Journal><ArticleTitle>[Inhibitors of RAS Might Be a Good Choice for the Therapy of COVID-19 Pneumonia].</ArticleTitle><Pagination><MedlinePgn>E014</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.3760/cma.j.issn.1001-0939.2020.0014</ELocationID><Abstract><AbstractText>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.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Sun</LastName><ForeName>M L</ForeName><Initials>ML</Initials><AffiliationInfo><Affiliation>Department of Oncology, Jinan Central Hospital Affiliated to Shandong University, Jinan 250013, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yang</LastName><ForeName>J M</ForeName><Initials>JM</Initials><AffiliationInfo><Affiliation>The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese Ministry of Health and Chinese Academy of Medical Sciences, Department of Cardiology, Qilu Hospital of Shandong University, Jinan 250012, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sun</LastName><ForeName>Y P</ForeName><Initials>YP</Initials><AffiliationInfo><Affiliation>Department of Oncology, Jinan Central Hospital Affiliated to Shandong University, Jinan 250013, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Su</LastName><ForeName>G H</ForeName><Initials>GH</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Jinan Central Hospital Affiliated to Shandong University, Jinan 250013, China.</Affiliation></AffiliationInfo></Author></AuthorList><Language>chi</Language><GrantList CompleteYN="Y"><Grant><GrantID>201907031</GrantID><Agency>Jinan Science and Technology Development Plan</Agency><Country></Country></Grant><Grant><GrantID>81570324, 81970366</GrantID><Agency>National Natural Science Foundation of China</Agency><Country></Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D004740">English Abstract</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2020</Year><Month>02</Month><Day>16</Day></ArticleDate></Article><MedlineJournalInfo><Country>China</Country><MedlineTA>Zhonghua Jie He He Hu Xi Za Zhi</MedlineTA><NlmUniqueID>8712226</NlmUniqueID><ISSNLinking>1001-0939</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><OtherAbstract Type="Publisher" Language="chi"><AbstractText>新型冠状病毒通过与人体血管紧张素转化酶2（ACE2）结合感染产生重症肺炎，传染性强，病死率高，目前无确切有效的治疗方式。ACE2是肾素-血管紧张素系统（RAS）的重要组成部分，RAS系统中ACE/Ang II/AT1R通路与ACE2/Ang (1-7)/Mas受体通路失衡将导致多系统炎症。ACE和Ang II升高是重症肺炎的不良预后因素。动物实验结果显示，应用RAS抑制剂可以有效缓解急性重症肺炎症状，缓解呼吸衰竭。新型冠状病毒与ACE2的结合导致ACE2耗竭，ACE2/Ang (1-7)/Mas受体通路受到抑制，RAS系统失衡，使新型冠状病毒肺炎患者病死率升高。因此，在控制血压的情况下，对新型冠状病毒肺炎患者应用ACEI及AT1R抑制剂，有可能减轻患者肺部炎症反应，降低患者病死率。.</AbstractText></OtherAbstract></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2020</Year><Month>2</Month><Day>16</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2020</Year><Month>2</Month><Day>16</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2020</Year><Month>2</Month><Day>16</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>aheadofprint</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">32061198</ArticleId><ArticleId IdType="doi">10.3760/cma.j.issn.1001-0939.2020.0014</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>République populaire de Chine</li></country></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Sun, M L" sort="Sun, M L" uniqKey="Sun M" first="M L" last="Sun">M L Sun</name></noRegion><name sortKey="Su, G H" sort="Su, G H" uniqKey="Su G" first="G H" last="Su">G H Su</name><name sortKey="Sun, Y P" sort="Sun, Y P" uniqKey="Sun Y" first="Y P" last="Sun">Y P Sun</name><name sortKey="Yang, J M" sort="Yang, J M" uniqKey="Yang J" first="J M" last="Yang">J M Yang</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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