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Review
. 2023 Mar 28;24(7):6390.
doi: 10.3390/ijms24076390.

The Role of Adipokines in the Pathogenesis of Psoriasis

Affiliations
Review

The Role of Adipokines in the Pathogenesis of Psoriasis

Kajetan Kiełbowski et al. Int J Mol Sci. .

Abstract

Psoriasis is a chronic and immune-mediated skin condition characterized by pro-inflammatory cytokines and keratinocyte hyperproliferation. Dendritic cells, T lymphocytes, and keratinocytes represent the main cell subtypes involved in the pathogenesis of psoriasis, while the interleukin-23 (IL-23)/IL-17 pathway enhances the disease progression. Human adipose tissue is an endocrine organ, which secretes multiple proteins, known as adipokines, such as adiponectin, leptin, visfatin, or resistin. Current evidence highlights the immunomodulatory roles of adipokines, which may contribute to the progression or suppression of psoriasis. A better understanding of the complexity of psoriasis pathophysiology linked with adipokines could result in developing novel diagnostic or therapeutic strategies. This review aims to present the pathogenesis of psoriasis and the roles of adipokines in this process.

Keywords: adipokines; adiponectin; cytokines; inflammation; leptin; psoriasis.

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Conflict of interest statement

The authors declare no conflicts of interest.

Figures

Figure 1
Figure 1
Schematic representation of the adiponectin isoforms and signaling. AdipoR1—adiponectin receptor 1; AdipoR2—adiponectin receptor 2; APPL—adaptor protein containing PH domain, PTB domain, and leucine zipper motif-1; AMPK—AMP-activated protein kinase; MAPK—mitogen-activated protein kinase; PPAR—peroxisome proliferator-activated receptor.
Figure 2
Figure 2
(A): Schematic representation of the pathogenesis of psoriasis and the roles of chemerin and adiponectin; (B): Impact of leptin on T cell variants; (C): Visfatin and TNF-α promote production of chemokines and antimicrobial peptides.
Figure 3
Figure 3
Schematic and simplified representation of the leptin signaling pathway. GRB2—growth factor receptor-bound protein 2; JAK2—janus kinase 2; MAPK—mitogen-activated protein kinase; PI3K—phosphoinositide 3-kinase; PIP2—phosphatidylinositol 4,5-biphosphate; SHP2—Src homology-2 domain-containing protein tyrosine phosphatase-2; STAT3—signal transducer and activator of transcription 3; STAT5—signal transducer and activator of transcription 5.

References

    1. Christophers E. Psoriasis-epidemiology and clinical spectrum. Clin. Exp. Dermatol. 2001;26:314–320. doi: 10.1046/j.1365-2230.2001.00832.x. - DOI - PubMed
    1. Danielsen K., Olsen A.O., Wilsgaard T., Furberg A.S. Is the prevalence of psoriasis increasing? A 30-year follow-up of a population-based cohort. Br. J. Dermatol. 2013;168:1303–1310. doi: 10.1111/bjd.12230. - DOI - PubMed
    1. Kubota K., Kamijima Y., Sato T., Ooba N., Koide D., Iizuka H., Nakagawa H. Epidemiology of psoriasis and palmoplantar pustulosis: A nationwide study using the Japanese national claims database. BMJ Open. 2015;5:e006450. doi: 10.1136/bmjopen-2014-006450. - DOI - PMC - PubMed
    1. Green A.C. Australian Aborigines and psoriasis. Australas. J. Dermatol. 1984;25:18–24. doi: 10.1111/j.1440-0960.1984.tb00618.x. - DOI - PubMed
    1. Huerta C., Rivero E., Rodríguez L.A. Incidence and risk factors for psoriasis in the general population. Arch. Dermatol. 2007;143:1559–1565. doi: 10.1001/archderm.143.12.1559. - DOI - PubMed