The IL-4/IL-13 axis in skin fibrosis and scarring: mechanistic concepts and therapeutic targets.
Cytokines
Interleukin-13
Interleukin-4
Scarring
Skin fibrosis
Journal
Archives of dermatological research
ISSN: 1432-069X
Titre abrégé: Arch Dermatol Res
Pays: Germany
ID NLM: 8000462
Informations de publication
Date de publication:
Mar 2020
Mar 2020
Historique:
received:
05
06
2019
accepted:
29
08
2019
revised:
22
07
2019
pubmed:
8
9
2019
medline:
28
10
2020
entrez:
8
9
2019
Statut:
ppublish
Résumé
Skin fibrosis, characterized by excessive fibroblast proliferation and extracellular matrix deposition in the dermis, is the histopathologic hallmark of dermatologic diseases such as systemic sclerosis, hypertrophic scars, and keloids. Effective anti-scarring therapeutics remain an unmet need, underscoring the complex pathophysiologic mechanisms of skin fibrosis. The Th2 cytokines interleukin (IL)-4 and IL-13 have been implicated as key mediators in the pathogenesis of fibroproliferative disorders. The goal of this article is to summarize the current understanding of the role of the IL-4/IL-13 axis in wound healing and skin fibrosis. We conducted a literature search to identify research studies investigating the roles of IL-4 and IL-13 in fibrotic skin diseases. While transforming growth factor-beta has long been regarded as the main driver of fibrotic processes, research into the cellular and molecular biology of wound healing has revealed other pathways that promote scar tissue formation. IL-4 and IL-13 are important mediators of skin fibrosis, supported by evidence from in vitro data, animal models of fibrosis, and clinical studies. Overactive signaling of the IL-4/IL-13 axis contributes to the initiation and perpetuation of fibrotic skin diseases. Further insights into the IL-4/IL-13 axis may reveal potential targets for the development of novel therapies that prevent or treat fibrotic skin diseases.
Identifiants
pubmed: 31493000
doi: 10.1007/s00403-019-01972-3
pii: 10.1007/s00403-019-01972-3
pmc: PMC7008089
mid: NIHMS1539245
doi:
Substances chimiques
IL4 protein, human
0
Interleukin-13
0
Interleukin-4
207137-56-2
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
81-92Subventions
Organisme : NIGMS NIH HHS
ID : K23 GM117309
Pays : United States
Organisme : NIGMS NIH HHS
ID : K23GM117309
Pays : United States
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