Twenty years of progress in angiotensin converting enzyme 2 and its link to SARS-CoV-2 disease

The virulence of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and the aggressive nature of the disease has transformed the universal pace of research in the desperate attempt to seek effective therapies to halt the morbidity and mortality of this pandemic. The rapid seq...

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Published inClinical science (1979) Vol. 134; no. 19; pp. 2645 - 2664
Main Authors Ferrario, Carlos M., Ahmad, Sarfaraz, Groban, Leanne
Format Journal Article
LanguageEnglish
Published England 16.10.2020
Subjects
Angiotensin-Converting Enzyme 2
Angiotensin-Converting Enzyme Inhibitors - pharmacology
Betacoronavirus - pathogenicity
Coronavirus Infections - drug therapy
Coronavirus Infections - enzymology
Coronavirus Infections - virology
COVID-19
Humans
Pandemics
Peptidyl-Dipeptidase A - drug effects
Peptidyl-Dipeptidase A - metabolism
Pneumonia, Viral - drug therapy
Pneumonia, Viral - enzymology
Pneumonia, Viral - virology
SARS-CoV-2
Time Factors
cardiovascular disease
angiotensin-(1-7)
coronavirus
innate immunity
angiotensin II
chymase
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Abstract The virulence of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and the aggressive nature of the disease has transformed the universal pace of research in the desperate attempt to seek effective therapies to halt the morbidity and mortality of this pandemic. The rapid sequencing of the SARS-CoV-2 virus facilitated identification of the receptor for angiotensin converting enzyme 2 (ACE2) as the high affinity binding site that allows virus endocytosis. Parallel evidence that coronavirus disease 2019 (COVID-19) disease evolution shows greater lethality in patients with antecedent cardiovascular disease, diabetes, or even obesity questioned the potential unfavorable contribution of angiotensin converting enzyme (ACE) inhibitors or angiotensin II (Ang II) receptor blockers as facilitators of adverse outcomes due to the ability of these therapies to augment the transcription of Ace2 with consequent increase in protein formation and enzymatic activity. We review, here, the specific studies that support a role of these agents in altering the expression and activity of ACE2 and underscore that the robustness of the experimental data is associated with weak clinical long-term studies of the existence of a similar regulation of tissue or plasma ACE2 in human subjects.
AbstractList The virulence of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and the aggressive nature of the disease has transformed the universal pace of research in the desperate attempt to seek effective therapies to halt the morbidity and mortality of this pandemic. The rapid sequencing of the SARS-CoV-2 virus facilitated identification of the receptor for angiotensin converting enzyme 2 (ACE2) as the high affinity binding site that allows virus endocytosis. Parallel evidence that coronavirus disease 2019 (COVID-19) disease evolution shows greater lethality in patients with antecedent cardiovascular disease, diabetes, or even obesity questioned the potential unfavorable contribution of angiotensin converting enzyme (ACE) inhibitors or angiotensin II (Ang II) receptor blockers as facilitators of adverse outcomes due to the ability of these therapies to augment the transcription of Ace2 with consequent increase in protein formation and enzymatic activity. We review, here, the specific studies that support a role of these agents in altering the expression and activity of ACE2 and underscore that the robustness of the experimental data is associated with weak clinical long-term studies of the existence of a similar regulation of tissue or plasma ACE2 in human subjects.
The virulence of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and the aggressive nature of the disease has transformed the universal pace of research in the desperate attempt to seek effective therapies to halt the morbidity and mortality of this pandemic. The rapid sequencing of the SARS-CoV-2 virus facilitated identification of the receptor for angiotensin converting enzyme 2 (ACE2) as the high affinity binding site that allows virus endocytosis. Parallel evidence that coronavirus disease 2019 (COVID-19) disease evolution shows greater lethality in patients with antecedent cardiovascular disease, diabetes, or even obesity questioned the potential unfavorable contribution of angiotensin converting enzyme (ACE) inhibitors or angiotensin II (Ang II) receptor blockers as facilitators of adverse outcomes due to the ability of these therapies to augment the transcription of Ace2 with consequent increase in protein formation and enzymatic activity. We review, here, the specific studies that support a role of these agents in altering the expression and activity of ACE2 and underscore that the robustness of the experimental data is associated with weak clinical long-term studies of the existence of a similar regulation of tissue or plasma ACE2 in human subjects.The virulence of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and the aggressive nature of the disease has transformed the universal pace of research in the desperate attempt to seek effective therapies to halt the morbidity and mortality of this pandemic. The rapid sequencing of the SARS-CoV-2 virus facilitated identification of the receptor for angiotensin converting enzyme 2 (ACE2) as the high affinity binding site that allows virus endocytosis. Parallel evidence that coronavirus disease 2019 (COVID-19) disease evolution shows greater lethality in patients with antecedent cardiovascular disease, diabetes, or even obesity questioned the potential unfavorable contribution of angiotensin converting enzyme (ACE) inhibitors or angiotensin II (Ang II) receptor blockers as facilitators of adverse outcomes due to the ability of these therapies to augment the transcription of Ace2 with consequent increase in protein formation and enzymatic activity. We review, here, the specific studies that support a role of these agents in altering the expression and activity of ACE2 and underscore that the robustness of the experimental data is associated with weak clinical long-term studies of the existence of a similar regulation of tissue or plasma ACE2 in human subjects.
The virulence of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and the aggressive nature of the disease has transformed the universal pace of research in the desperate attempt to seek effective therapies to halt the morbidity and mortality of this pandemic. The rapid sequencing of the SARS-CoV-2 virus facilitated identification of the receptor for angiotensin converting enzyme 2 (ACE2) as the high affinity binding site that allows virus endocytosis. Parallel evidence that coronavirus disease 2019 (COVID-19) disease evolution shows greater lethality in patients with antecedent cardiovascular disease, diabetes, or even obesity questioned the potential unfavorable contribution of angiotensin converting enzyme (ACE) inhibitors or angiotensin II (Ang II) receptor blockers as facilitators of adverse outcomes due to the ability of these therapies to augment the transcription of Ace2 with consequent increase in protein formation and enzymatic activity. We review, here, the specific studies that support a role of these agents in altering the expression and activity of ACE2 and underscore that the robustness of the experimental data is associated with weak clinical long-term studies of the existence of a similar regulation of tissue or plasma ACE2 in human subjects.
Author Ferrario, Carlos M.
Groban, Leanne
Ahmad, Sarfaraz
AuthorAffiliation 2 Department of Surgery, Wake Forest School of Medicine, Winston-Salem, NC 27157, U.S.A
3 Department of Anesthesiology, Wake Forest School of Medicine, Winston-Salem, NC 27157, U.S.A
1 Departments of Surgery and Physiology-Pharmacology, Wake Forest School of Medicine, Winston-Salem, NC 27157, U.S.A
AuthorAffiliation_xml – name: 3 Department of Anesthesiology, Wake Forest School of Medicine, Winston-Salem, NC 27157, U.S.A
– name: 1 Departments of Surgery and Physiology-Pharmacology, Wake Forest School of Medicine, Winston-Salem, NC 27157, U.S.A
– name: 2 Department of Surgery, Wake Forest School of Medicine, Winston-Salem, NC 27157, U.S.A
Author_xml – sequence: 1
  givenname: Carlos M.
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Keywords cardiovascular disease
angiotensin-(1-7)
coronavirus
innate immunity
angiotensin II
chymase
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Snippet The virulence of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and the aggressive nature of the disease has transformed the...
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SubjectTerms Angiotensin-Converting Enzyme 2
Angiotensin-Converting Enzyme Inhibitors - pharmacology
Betacoronavirus - pathogenicity
Coronavirus Infections - drug therapy
Coronavirus Infections - enzymology
Coronavirus Infections - virology
COVID-19
Humans
Pandemics
Peptidyl-Dipeptidase A - drug effects
Peptidyl-Dipeptidase A - metabolism
Pneumonia, Viral - drug therapy
Pneumonia, Viral - enzymology
Pneumonia, Viral - virology
SARS-CoV-2
Time Factors
Title Twenty years of progress in angiotensin converting enzyme 2 and its link to SARS-CoV-2 disease
URI https://www.ncbi.nlm.nih.gov/pubmed/33063823
https://www.proquest.com/docview/2451859078
https://pubmed.ncbi.nlm.nih.gov/PMC9055624
Volume 134
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