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PDE4 inhibition as a therapeutic strategy for improvement of pulmonary dysfunctions in Covid-19 and cigarette smoking

Authors
  • Lugnier, Claire1
  • Al-Kuraishy, Hayder M.2
  • Rousseau, Eric3
  • 1 Directeur de Recherche 1 CNRS/université de Strasbourg, Institut de Physiologie, Faculté de Médecine, CRBS, UR3072: “Mitochondrie, stress oxydant et protection musculaire”, 1 rue Eugène Boeckel, 67000 Strasbourg, France
  • 2 Medical Faculty College of Medicine, Al-Mustansiriya University, P.O. Box 14132, Baghdad, Iraq
  • 3 Department of Obstetrics and Gynecology, Faculty of Medicine and Health Sciences, Université de Sherbrooke, and Centre de Recherche du CHUS, Sherbrooke, QC, Canada
Type
Published Article
Journal
Biochemical pharmacology
Publisher
New York, NY : Elsevier Science Inc
Publication Date
Jan 28, 2021
Volume
185
Pages
114431–114431
Identifiers
DOI: 10.1016/j.bcp.2021.114431
PMID: 33515531
PMCID: PMC7842152
Source
PubMed Central
Keywords
Disciplines
  • Review
License
Unknown

Abstract

Angiotensin-converting enzyme 2 (ACE2) is the binding-site and entry-point for SARS-CoV-2 in human and highly expressed in the lung. Cigarette smoking (CS) is the leading cause of pulmonary and cardiovascular diseases. Chronic CS leads to upregulation of bronchial ACE2 inducing a high vulnerability in COVID-19 smoker patients. Interestingly, CS-induced dysregulation of pulmonary renin-angiotensin system (RAS) in part contributing into the potential pathogenesis COVID-19 pneumonia and acute respiratory distress syndrome (ARDS). Since, CS-mediated ACE2 activations is not the main pathway for increasing the risk of COVID-19, it appeared that AngII/AT1R might induce an inflammatory-burst in COVID-19 response by up-regulating cyclic nucleotide phosphodiesterase type 4 (PDE4), which hydrolyses specifically the second intracellular messenger 3′, 5′-cyclic AMP (cAMP). It must be pointed out that CS might induce PDE4 up-regulation similarly to the COVID-19 inflammation, and therefore could potentiate COVID-19 inflammation opening the potential therapeutic effects of PDE4 inhibitor in both COVID-19-inflammation and CS.

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