DPP4 inhibition: Preventing SARS-CoV-2 infection and/or progression of COVID-19?
CD26
COVID-19
DPP4 inhibitors
SARS-CoV-2
coronavirus
dipeptidyl peptidase 4
Journal
Diabetes/metabolism research and reviews
ISSN: 1520-7560
Titre abrégé: Diabetes Metab Res Rev
Pays: England
ID NLM: 100883450
Informations de publication
Date de publication:
11 2020
11 2020
Historique:
received:
09
04
2020
revised:
16
04
2020
accepted:
20
04
2020
pubmed:
27
4
2020
medline:
1
12
2020
entrez:
27
4
2020
Statut:
ppublish
Résumé
Dipeptidyl peptidase 4 (DPP4), also known as cluster of differentiation 26 (CD26), is a serine exopeptidase expressed ubiquitously in several tissues, including but not limited to lung, kidney, liver, gut, and immune cells. The question has been raised on whether DPP4 modulation or inhibition may prevent infection and/or progression of the COVID-19. A docked complex model of the SARS-CoV-2 spike glycoprotein and DPP4 has been proposed, showing a large interface between the proteins and proposing close similarity with other coronaviruses using DPP4 as functional receptor. In absence of experimental validation, these data should be interpreted with caution. Nevertheless, this observation may rise the question on whether DPP4 is directly involved in SARS-CoV-2 cell adhesion/virulence, and whether DPP4 inhibition might be a therapeutic strategy for preventing infection. Although a direct involvement of DPP4 in SARS-CoV-2 infection needs to be clarified, there is also evidence suggesting that DPP4 inhibitors modulate inflammation and exert anti-fibrotic activity. These properties may be of potential use for halting progression to the hyperinflammatory state associated with severe COVID-19. Taken together these findings may suggest a potential role for DPP4 inhibition or modulation in one or more steps of COVID-19 immunopathogenesis.
Identifiants
pubmed: 32336007
doi: 10.1002/dmrr.3330
pmc: PMC7267128
doi:
Substances chimiques
Dipeptidyl-Peptidase IV Inhibitors
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
e3330Informations de copyright
© 2020 John Wiley & Sons Ltd.
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