The pivotal link between ACE2 deficiency and SARS-CoV-2 infection
Identifieur interne : 000086 ( 2020/Analysis ); précédent : 000085; suivant : 000087The pivotal link between ACE2 deficiency and SARS-CoV-2 infection
Auteurs : Paolo Verdecchia ; Claudio Cavallini ; Antonio Spanevello ; Fabio AngeliSource :
- European Journal of Internal Medicine [ 0953-6205 ] ; 2020.
Abstract
Angiotensin converting enzyme-2 (ACE2) receptors mediate the entry into the cell of three strains of coronavirus: SARS-CoV, NL63 and SARS-CoV-2. ACE2 receptors are ubiquitous and widely expressed in the heart, vessels, gut, lung (particularly in type 2 pneumocytes and macrophages), kidney, testis and brain. ACE2 is mostly bound to cell membranes and only scarcely present in the circulation in a soluble form. An important salutary function of membrane-bound and soluble ACE2 is the degradation of angiotensin II to angiotensin1-7. Consequently, ACE2 receptors limit several detrimental effects resulting from binding of angiotensin II to AT1 receptors, which include vasoconstriction, enhanced inflammation and thrombosis. The increased generation of angiotensin1-7 also triggers counter-regulatory protective effects through binding to G-protein coupled Mas receptors. Unfortunately, the entry of SARS-CoV2 into the cells through membrane fusion markedly down-regulates ACE2 receptors, with loss of the catalytic effect of these receptors at the external site of the membrane. Increased pulmonary inflammation and coagulation have been reported as unwanted effects of enhanced and unopposed angiotensin II effects via the ACE→Angiotensin II→AT1 receptor axis. Clinical reports of patients infected with SARS-CoV-2 show that several features associated with infection and severity of the disease (i.e., older age, hypertension, diabetes, cardiovascular disease) share a variable degree of ACE2 deficiency. We suggest that ACE2 down-regulation induced by viral invasion may be especially detrimental in people with baseline ACE2 deficiency associated with the above conditions. The additional ACE2 deficiency after viral invasion might amplify the dysregulation between the ‘adverse’ ACE→Angiotensin II→AT1 receptor axis and the ‘protective’ ACE2→Angiotensin1-7→Mas receptor axis. In the lungs, such dysregulation would favor the progression of inflammatory and thrombotic processes triggered by local angiotensin II hyperactivity unopposed by angiotensin1-7. In this setting, recombinant ACE2, angiotensin1-7 and angiotensin II type 1 receptor blockers could be promising therapeutic approaches in patients with SARS-CoV-2 infection.
Url:
DOI: 10.1016/j.ejim.2020.04.037
PubMed: 32336612
PubMed Central: 7167588
Affiliations:
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Maria della Misericordia, Perugia.</nlm:aff><wicri:noCountry code="subfield">Perugia.</wicri:noCountry></affiliation></author><author><name sortKey="Cavallini, Claudio" sort="Cavallini, Claudio" uniqKey="Cavallini C" first="Claudio" last="Cavallini">Claudio Cavallini</name><affiliation><nlm:aff id="aff0001">Fondazione Umbra Cuore e Ipertensione-ONLUS and Struttura Complessa di Cardiologia, Ospedale S. Maria della Misericordia, Perugia.</nlm:aff><wicri:noCountry code="subfield">Perugia.</wicri:noCountry></affiliation></author><author><name sortKey="Spanevello, Antonio" sort="Spanevello, Antonio" uniqKey="Spanevello A" first="Antonio" last="Spanevello">Antonio Spanevello</name><affiliation><nlm:aff id="aff0002">Dipartimento di Medicina e Chirurgia, Università degli Studi dell'Insubria, Varese</nlm:aff><wicri:noCountry code="subfield">Varese</wicri:noCountry></affiliation><affiliation><nlm:aff id="aff0003">Dipartimento di Medicina e Riabilitazione Cardio-Respiratoria, Istituti Clinici Scientici Maugeri, IRCCS Tradate (VA)</nlm:aff><wicri:noCountry code="subfield">IRCCS Tradate (VA)</wicri:noCountry></affiliation></author><author><name sortKey="Angeli, Fabio" sort="Angeli, Fabio" uniqKey="Angeli F" first="Fabio" last="Angeli">Fabio Angeli</name><affiliation><nlm:aff id="aff0002">Dipartimento di Medicina e Chirurgia, Università degli Studi dell'Insubria, Varese</nlm:aff><wicri:noCountry code="subfield">Varese</wicri:noCountry></affiliation><affiliation><nlm:aff id="aff0003">Dipartimento di Medicina e Riabilitazione Cardio-Respiratoria, Istituti Clinici Scientici Maugeri, IRCCS Tradate (VA)</nlm:aff><wicri:noCountry code="subfield">IRCCS Tradate (VA)</wicri:noCountry></affiliation></author></analytic><series><title level="j">European Journal of Internal Medicine</title><idno type="ISSN">0953-6205</idno><idno type="eISSN">1879-0828</idno><imprint><date when="2020">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Angiotensin converting enzyme-2 (ACE2) receptors mediate the entry into the cell of three strains of coronavirus: SARS-CoV, NL63 and SARS-CoV-2. ACE2 receptors are ubiquitous and widely expressed in the heart, vessels, gut, lung (particularly in type 2 pneumocytes and macrophages), kidney, testis and brain. ACE2 is mostly bound to cell membranes and only scarcely present in the circulation in a soluble form. An important salutary function of membrane-bound and soluble ACE2 is the degradation of angiotensin II to angiotensin<sub>1-7</sub>. Consequently, ACE2 receptors limit several detrimental effects resulting from binding of angiotensin II to AT1 receptors, which include vasoconstriction, enhanced inflammation and thrombosis. The increased generation of angiotensin<sub>1-7</sub> also triggers counter-regulatory protective effects through binding to G-protein coupled Mas receptors. Unfortunately, the entry of SARS-CoV2 into the cells through membrane fusion markedly down-regulates ACE2 receptors, with loss of the catalytic effect of these receptors at the external site of the membrane. Increased pulmonary inflammation and coagulation have been reported as unwanted effects of enhanced and unopposed angiotensin II effects via the ACE→Angiotensin II→AT1 receptor axis. Clinical reports of patients infected with SARS-CoV-2 show that several features associated with infection and severity of the disease (i.e., older age, hypertension, diabetes, cardiovascular disease) share a variable degree of ACE2 deficiency. We suggest that ACE2 down-regulation induced by viral invasion may be especially detrimental in people with baseline ACE2 deficiency associated with the above conditions. The additional ACE2 deficiency after viral invasion might amplify the dysregulation between the ‘adverse’ ACE→Angiotensin II→AT1 receptor axis and the ‘protective’ ACE2→Angiotensin<sub>1-7</sub>→Mas receptor axis. In the lungs, such dysregulation would favor the progression of inflammatory and thrombotic processes triggered by local angiotensin II hyperactivity unopposed by angiotensin<sub>1-7</sub>. In this setting, recombinant ACE2, angiotensin<sub>1-7</sub> and angiotensin II type 1 receptor blockers could be promising therapeutic approaches in patients with SARS-CoV-2 infection.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Chan Yeung, M" uniqKey="Chan Yeung M">M Chan-Yeung</name></author><author><name sortKey="Xu, Rh" uniqKey="Xu R">RH. 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Gurwitz</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Kuster, Gm" uniqKey="Kuster G">GM Kuster</name></author><author><name sortKey="Pfister, O" uniqKey="Pfister O">O Pfister</name></author><author><name sortKey="Burkard, T" uniqKey="Burkard T">T Burkard</name></author><author><name sortKey="Zhou, Q" uniqKey="Zhou Q">Q Zhou</name></author><author><name sortKey="Twerenbold, R" uniqKey="Twerenbold R">R Twerenbold</name></author><author><name sortKey="Haaf, P" uniqKey="Haaf P">P Haaf</name></author><author><name sortKey="Widmer, Af" uniqKey="Widmer A">AF Widmer</name></author><author><name sortKey="Osswald, S" uniqKey="Osswald S">S Osswald</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Vaduganathan, M" uniqKey="Vaduganathan M">M Vaduganathan</name></author><author><name sortKey="Vardeny, O" uniqKey="Vardeny O">O Vardeny</name></author><author><name sortKey="Michel, T" uniqKey="Michel T">T Michel</name></author><author><name sortKey="Mcmurray, Jjv" uniqKey="Mcmurray J">JJV McMurray</name></author><author><name sortKey="Pfeffer, Ma" uniqKey="Pfeffer M">MA Pfeffer</name></author><author><name sortKey="Solomon, Sd" uniqKey="Solomon S">SD Solomon</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Verdecchia, P" uniqKey="Verdecchia P">P Verdecchia</name></author><author><name sortKey="Angeli, F" uniqKey="Angeli F">F Angeli</name></author><author><name sortKey="Reboldi, G" uniqKey="Reboldi G">G Reboldi</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Verdecchia, P" uniqKey="Verdecchia P">P Verdecchia</name></author><author><name sortKey="Reboldi, G" uniqKey="Reboldi G">G Reboldi</name></author><author><name sortKey="Cavallini, C" uniqKey="Cavallini C">C Cavallini</name></author><author><name sortKey="Mazzotta, G" uniqKey="Mazzotta G">G Mazzotta</name></author><author><name sortKey="Angeli, F" uniqKey="Angeli F">F Angeli</name></author></analytic></biblStruct></listBibl></div1></back></TEI><affiliations><list></list><tree><noCountry><name sortKey="Angeli, Fabio" sort="Angeli, Fabio" uniqKey="Angeli F" first="Fabio" last="Angeli">Fabio Angeli</name><name sortKey="Cavallini, Claudio" sort="Cavallini, Claudio" uniqKey="Cavallini C" first="Claudio" last="Cavallini">Claudio Cavallini</name><name sortKey="Spanevello, Antonio" sort="Spanevello, Antonio" uniqKey="Spanevello A" first="Antonio" last="Spanevello">Antonio Spanevello</name><name sortKey="Verdecchia, Paolo" sort="Verdecchia, Paolo" uniqKey="Verdecchia P" first="Paolo" last="Verdecchia">Paolo Verdecchia</name></noCountry></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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