Interleukin-13 (IL-13) - A Pleiotropic Cytokine Involved in Wound Healing and Fibrosis

dc.contributor.authorRoeb, Elke
dc.date.accessioned2024-02-07T14:38:47Z
dc.date.available2024-02-07T14:38:47Z
dc.date.issued2023
dc.description.abstractThe liver, as a central metabolic organ, is systemically linked to metabolic–inflammatory diseases. In the pathogenesis of the metabolic syndrome, inflammatory and metabolic interactions between the intestine, liver, and adipose tissue lead to the progression of hepatic steatosis to metabolic-dysfunction-associated steatohepatitis (MASH) and consecutive MASH-induced fibrosis. Clinical and animal studies revealed that IL-13 might be protective in the development of MASH through both the preservation of metabolic functions and Th2-polarized inflammation in the liver and the adipose tissue. In contrast, IL-13-associated loss of mucosal gut barrier function and IL-13-associated enhanced hepatic fibrosis may contribute to the progression of MASH. However, there are only a few publications on the effect of IL-13 on metabolic diseases and possible therapies to influence them. In this review article, different aspects of IL-13-associated effects on the liver and metabolic liver diseases, which are partly contradictory, are summarized and discussed on the basis of the recent literature.
dc.description.sponsorshipDeutsche Forschungsgemeinschaft (DFG); ROR-ID:018mejw64
dc.identifier.urihttps://jlupub.ub.uni-giessen.de//handle/jlupub/18993
dc.identifier.urihttp://dx.doi.org/10.22029/jlupub-18354
dc.language.isoen
dc.rightsNamensnennung 4.0 International
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.subject.ddcddc:610
dc.titleInterleukin-13 (IL-13) - A Pleiotropic Cytokine Involved in Wound Healing and Fibrosis
dc.typearticle
local.affiliationFB 11 - Medizin
local.projectGrant number RO957/13-1 and RO3714/4-1
local.source.articlenumber12884
local.source.epage12
local.source.journaltitleInternational journal of molecular sciences
local.source.spage1
local.source.urihttps://doi.org/10.3390/ijms241612884
local.source.volume24

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