Summary

Psoriasis is a chronic inflammatory skin disorder with a complex autoimmune basis, characterized by keratinocyte hyperproliferation and a dermo-epidermal inflammatory infiltrate. Conversely, obesity represents a metabolic condition defined by the excessive accumulation of adipose tissue and is increasingly acknowledged as a state of low-grade chronic inflammation. In recent years, a strong bidirectional association between these two entities has emerged, suggesting the existence of a vicious cycle wherein systemic inflammation associated with obesity exacerbates psoriasis, and vice versa.

Adipose tissue secretes a range of proinflammatory cytokines, collectively termed adipokines – including tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), leptin, and resistin – which contribute to a systemic pro-inflammatory milieu that may potentiate autoimmune disorders such as psoriasis. Furthermore, psoriasis itself is associated with elevated levels of inflammatory mediators that can disrupt metabolic homeostasis and promote visceral adiposity, thereby further aggravating obesity. This intricate interplay bears significant clinical relevance, impacting therapeutic responses, disease prognosis, and the risk of cardiovascular comorbidities.

Psoriasis and obesity thus share a common inflam-matory pathogenesis, and elucidating the molecular pathways linking these conditions could foster the development of more effective, personalized therapeutic strategies targeting systemic inflammation in an integrated manner.

This review aims to synthesize the current under-standing of the pathogenic role of adipokines and to explore the potential mechanisms through which inflammatory processes mediate the association between obesity and psoriasis.