ACE2 and COVID-19: using antihypertensive medications and pharmacogenetic considerations
COVID-19 utilizes the ACE2 pathway as a means of infection. Early data on COVID-19 suggest heterogeneity in the severity of symptoms during transmission and infection ranging from no symptoms to death. The source of this heterogeneity is likely multifaceted and may have a genetic component. Demograp...
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| Veröffentlicht in: | Pharmacogenomics 2020-07, Vol.21 (10), p.695-703 |
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| creator | Snyder, Eric M Johnson, Bruce D |
| description | COVID-19 utilizes the ACE2 pathway as a means of infection. Early data on COVID-19 suggest heterogeneity in the severity of symptoms during transmission and infection ranging from no symptoms to death. The source of this heterogeneity is likely multifaceted and may have a genetic component. Demographic and clinical comorbidities associated with the severity of infection suggest that possible variants known to influence the renin–angiotensin–aldosterone (RAAS) system pathway (particularly those that influence ACE2) may contribute to the heterogenous infection response. ACE2 and Ang(1–7) (the product of ACE2) seem to have a protective effect on the pulmonary and cardiac systems. Hypertension medication modulation, may alter ACE2 and Ang(1–7), particularly in variants that have been shown to influence RAAS system function, which could be clinically useful in patients with COVID-19. |
| doi_str_mv | 10.2217/pgs-2020-0048 |
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Early data on COVID-19 suggest heterogeneity in the severity of symptoms during transmission and infection ranging from no symptoms to death. The source of this heterogeneity is likely multifaceted and may have a genetic component. Demographic and clinical comorbidities associated with the severity of infection suggest that possible variants known to influence the renin–angiotensin–aldosterone (RAAS) system pathway (particularly those that influence ACE2) may contribute to the heterogenous infection response. ACE2 and Ang(1–7) (the product of ACE2) seem to have a protective effect on the pulmonary and cardiac systems. Hypertension medication modulation, may alter ACE2 and Ang(1–7), particularly in variants that have been shown to influence RAAS system function, which could be clinically useful in patients with COVID-19.</description><identifier>ISSN: 1462-2416</identifier><identifier>EISSN: 1744-8042</identifier><identifier>DOI: 10.2217/pgs-2020-0048</identifier><identifier>PMID: 32501190</identifier><language>eng</language><publisher>England: Future Medicine Ltd</publisher><subject>ACE-inhibition ; ACE2 ; Aldosterone ; Angiotensin ; Angiotensin II Type 1 Receptor Blockers - therapeutic use ; Angiotensin-Converting Enzyme 2 ; angiotensin-receptor blockade ; angiotensinogen ; Animals ; Antihypertensive Agents - therapeutic use ; Antihypertensives ; Blood pressure ; cardiac dysfunction ; coronavirus ; Coronavirus Infections - drug therapy ; Coronavirus Infections - genetics ; Coronaviruses ; COVID-19 ; Diabetes ; Disease transmission ; genomics ; Humans ; Hypertension ; Infections ; Influence ; Males ; Pandemics ; Peptidyl-Dipeptidase A - drug effects ; Peptidyl-Dipeptidase A - genetics ; Pharmacogenetics ; Pharmacogenomic Testing ; Pneumonia, Viral - drug therapy ; Pneumonia, Viral - genetics ; Proteins ; Renin ; Renin-Angiotensin System - drug effects ; respiratory failure ; Review ; Sheep ; Viral infections</subject><ispartof>Pharmacogenomics, 2020-07, Vol.21 (10), p.695-703</ispartof><rights>2020 Future Medicine Ltd</rights><rights>Copyright Future Medicine Ltd Jul 2020</rights><rights>2020 Future Medicine Ltd 2020</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c493t-7cadd43c6e0f31eb06321960a46e66ba990fc287a4c9934589de68a2b0bad6b33</citedby><cites>FETCH-LOGICAL-c493t-7cadd43c6e0f31eb06321960a46e66ba990fc287a4c9934589de68a2b0bad6b33</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7373206/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7373206/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32501190$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Snyder, Eric M</creatorcontrib><creatorcontrib>Johnson, Bruce D</creatorcontrib><title>ACE2 and COVID-19: using antihypertensive medications and pharmacogenetic considerations</title><title>Pharmacogenomics</title><addtitle>Pharmacogenomics</addtitle><description>COVID-19 utilizes the ACE2 pathway as a means of infection. Early data on COVID-19 suggest heterogeneity in the severity of symptoms during transmission and infection ranging from no symptoms to death. The source of this heterogeneity is likely multifaceted and may have a genetic component. Demographic and clinical comorbidities associated with the severity of infection suggest that possible variants known to influence the renin–angiotensin–aldosterone (RAAS) system pathway (particularly those that influence ACE2) may contribute to the heterogenous infection response. ACE2 and Ang(1–7) (the product of ACE2) seem to have a protective effect on the pulmonary and cardiac systems. Hypertension medication modulation, may alter ACE2 and Ang(1–7), particularly in variants that have been shown to influence RAAS system function, which could be clinically useful in patients with COVID-19.</description><subject>ACE-inhibition</subject><subject>ACE2</subject><subject>Aldosterone</subject><subject>Angiotensin</subject><subject>Angiotensin II Type 1 Receptor Blockers - therapeutic use</subject><subject>Angiotensin-Converting Enzyme 2</subject><subject>angiotensin-receptor blockade</subject><subject>angiotensinogen</subject><subject>Animals</subject><subject>Antihypertensive Agents - therapeutic use</subject><subject>Antihypertensives</subject><subject>Blood pressure</subject><subject>cardiac dysfunction</subject><subject>coronavirus</subject><subject>Coronavirus Infections - drug therapy</subject><subject>Coronavirus Infections - genetics</subject><subject>Coronaviruses</subject><subject>COVID-19</subject><subject>Diabetes</subject><subject>Disease transmission</subject><subject>genomics</subject><subject>Humans</subject><subject>Hypertension</subject><subject>Infections</subject><subject>Influence</subject><subject>Males</subject><subject>Pandemics</subject><subject>Peptidyl-Dipeptidase A - drug effects</subject><subject>Peptidyl-Dipeptidase A - genetics</subject><subject>Pharmacogenetics</subject><subject>Pharmacogenomic Testing</subject><subject>Pneumonia, Viral - drug therapy</subject><subject>Pneumonia, Viral - genetics</subject><subject>Proteins</subject><subject>Renin</subject><subject>Renin-Angiotensin System - drug effects</subject><subject>respiratory failure</subject><subject>Review</subject><subject>Sheep</subject><subject>Viral infections</subject><issn>1462-2416</issn><issn>1744-8042</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp1kUlP3DAUgC1UBHTokWsVqZdeDM_LOHEPSGjKJiFxKVVvluO8zBjNOMFOkPj39RCKAKknL-_zW_wRcsTgmHNWnvTLRDlwoACy2iEHrJSSViD5p7yXilMumdonn1O6B-BMSdgj-4LPgTENB-TP2eKcFzY0xeL29_VPyvSPYkw-LPPd4FdPPcYBQ_KPWGyw8c4Ovgvp-UG_snFjXbfEgIN3hcsB32CckEOy29p1wi8v64zcXZz_WlzRm9vL68XZDXVSi4GWzjaNFE4htIJhDUpwphVYqVCp2moNreNVaaXTWsh5pRtUleU11LZRtRAzcjrl7cc6d-gwDNGuTR_9xsYn01lv3keCX5ll92hKUQqey83I95cEsXsYMQ1m45PD9doG7MZk8v-BkCXMeUa_fUDvuzGGPF6mBK-EkFWZKTpRLnYpRWxfm2Fgts5Mdma2zszWWea_vp3glf4nKQN6AtpxGCMm5zE4NNPp2YoP-J_kfwGcKaYj</recordid><startdate>20200701</startdate><enddate>20200701</enddate><creator>Snyder, Eric M</creator><creator>Johnson, Bruce D</creator><general>Future Medicine Ltd</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>EHMNL</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20200701</creationdate><title>ACE2 and COVID-19: using antihypertensive medications and pharmacogenetic considerations</title><author>Snyder, Eric M ; Johnson, Bruce D</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c493t-7cadd43c6e0f31eb06321960a46e66ba990fc287a4c9934589de68a2b0bad6b33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>ACE-inhibition</topic><topic>ACE2</topic><topic>Aldosterone</topic><topic>Angiotensin</topic><topic>Angiotensin II Type 1 Receptor Blockers - therapeutic use</topic><topic>Angiotensin-Converting Enzyme 2</topic><topic>angiotensin-receptor blockade</topic><topic>angiotensinogen</topic><topic>Animals</topic><topic>Antihypertensive Agents - therapeutic use</topic><topic>Antihypertensives</topic><topic>Blood pressure</topic><topic>cardiac dysfunction</topic><topic>coronavirus</topic><topic>Coronavirus Infections - drug therapy</topic><topic>Coronavirus Infections - genetics</topic><topic>Coronaviruses</topic><topic>COVID-19</topic><topic>Diabetes</topic><topic>Disease transmission</topic><topic>genomics</topic><topic>Humans</topic><topic>Hypertension</topic><topic>Infections</topic><topic>Influence</topic><topic>Males</topic><topic>Pandemics</topic><topic>Peptidyl-Dipeptidase A - drug effects</topic><topic>Peptidyl-Dipeptidase A - genetics</topic><topic>Pharmacogenetics</topic><topic>Pharmacogenomic Testing</topic><topic>Pneumonia, Viral - drug therapy</topic><topic>Pneumonia, Viral - genetics</topic><topic>Proteins</topic><topic>Renin</topic><topic>Renin-Angiotensin System - drug effects</topic><topic>respiratory failure</topic><topic>Review</topic><topic>Sheep</topic><topic>Viral infections</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Snyder, Eric M</creatorcontrib><creatorcontrib>Johnson, Bruce D</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>UK & Ireland Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Pharmacogenomics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Snyder, Eric M</au><au>Johnson, Bruce D</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>ACE2 and COVID-19: using antihypertensive medications and pharmacogenetic considerations</atitle><jtitle>Pharmacogenomics</jtitle><addtitle>Pharmacogenomics</addtitle><date>2020-07-01</date><risdate>2020</risdate><volume>21</volume><issue>10</issue><spage>695</spage><epage>703</epage><pages>695-703</pages><issn>1462-2416</issn><eissn>1744-8042</eissn><abstract>COVID-19 utilizes the ACE2 pathway as a means of infection. Early data on COVID-19 suggest heterogeneity in the severity of symptoms during transmission and infection ranging from no symptoms to death. The source of this heterogeneity is likely multifaceted and may have a genetic component. Demographic and clinical comorbidities associated with the severity of infection suggest that possible variants known to influence the renin–angiotensin–aldosterone (RAAS) system pathway (particularly those that influence ACE2) may contribute to the heterogenous infection response. ACE2 and Ang(1–7) (the product of ACE2) seem to have a protective effect on the pulmonary and cardiac systems. Hypertension medication modulation, may alter ACE2 and Ang(1–7), particularly in variants that have been shown to influence RAAS system function, which could be clinically useful in patients with COVID-19.</abstract><cop>England</cop><pub>Future Medicine Ltd</pub><pmid>32501190</pmid><doi>10.2217/pgs-2020-0048</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | ACE-inhibition ACE2 Aldosterone Angiotensin Angiotensin II Type 1 Receptor Blockers - therapeutic use Angiotensin-Converting Enzyme 2 angiotensin-receptor blockade angiotensinogen Animals Antihypertensive Agents - therapeutic use Antihypertensives Blood pressure cardiac dysfunction coronavirus Coronavirus Infections - drug therapy Coronavirus Infections - genetics Coronaviruses COVID-19 Diabetes Disease transmission genomics Humans Hypertension Infections Influence Males Pandemics Peptidyl-Dipeptidase A - drug effects Peptidyl-Dipeptidase A - genetics Pharmacogenetics Pharmacogenomic Testing Pneumonia, Viral - drug therapy Pneumonia, Viral - genetics Proteins Renin Renin-Angiotensin System - drug effects respiratory failure Review Sheep Viral infections |
| title | ACE2 and COVID-19: using antihypertensive medications and pharmacogenetic considerations |
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