Resistin – A Plausible Therapeutic Target in the Pathogenesis of Psoriasis

ABSTRACT

Resistin, a cytokine hormone predominantly secreted by adipose tissue, is elevated in various metabolic disorders such as obesity, type 2 diabetes, and cardiovascular disease. In addition to its involvement in metabolic regulation, resistin has been implicated in the pathogenesis of psoriasis, a chronic inflammatory skin disorder. Numerous studies have reported increased resistin levels in psoriatic skin lesions, suggesting a possible association between resistin and psoriasis. Recent studies have suggested the potential involvement of resistin in the development and progression of certain cancers. Resistin is overexpressed in breast, colorectal, and gastric cancers. This suggests that it may play a role in the development of these cancers, possibly by inducing inflammation and cell growth. The link between resistin and cancer raises the possibility of shared underlying mechanisms driving the pathogenesis of psoriasis. Chronic inflammation, one such mechanism, is a hallmark of psoriasis and cancer. Further research is needed to fully understand the relationship between resistin and psoriasis. Identifying potential therapeutic targets is crucial for effective management of psoriasis. By doing so, we may be able to develop more effective treatment options for individuals living with psoriasis and ultimately improve their quality of life. Ultimately, a more comprehensive understanding of the mechanisms underlying the impact of resistin on psoriasis is essential for advancing our knowledge and finding new ways to treat and manage this challenging condition.

KEYWORDS:

• Diabetes
• keratinocyte
• leukocyte
• psoriasis
• resistin

Disclosure statement

No potential conflict of interest was reported by the author(s).

Author’s contributions

MS: Conceptualization, Literature collection, Writing – original draft preparation, SS: Conceptualization, Writing – review & editing. MR: Writing – review & editing Supervision.

Additional information

Funding

This work was not supported by any funding.