Aim of the review: Psoriasis is increasingly recognized as a systemic inflammatory disease frequently associated with a cluster of cardiometabolic comorbidities, including obesity, type 2 diabetes, and cardiovascular disease. Central to this association is the interleukin-17 (IL-17) signaling axis, a key driver of both cutaneous inflammation and systemic metabolic dysfunction. Materials and methods: This review examines the complex immunometabolic interactions mediated by IL-17 and synergistic cytokines such as TNF‑α, IL‑6, IL‑1β, IL‑23, and adipokines, which contribute to endothelial dysfunction, insulin resistance, and adipose-tissue inflammation. Results: Beyond its established role in psoriasis pathogenesis, the IL-17 pathway is implicated in the 'psoriatic march,' linking chronic skin inflammation to accelerated atherosclerosis. The advent of IL-17 inhibitors has transformed the management of moderate-to-severe psoriasis, achieving unprecedented skin clearance (PASI 90/100). Emerging evidence suggests that these agents may also exert potential beneficial effects on selected inflammatory and cardiometabolic markers. However, their direct impact on metabolic parameters remains under investigation. Conclusion: Understanding these shared molecular pathways is essential for adopting a holistic therapeutic approach that addresses both cutaneous disease and the systemic burden of psoriatic patients.
Unveiling the IL-17 axis: an immunometabolic bridge between psoriasis and metabolic syndrome
Carugno, AndreaUltimo
2026-01-01
Abstract
Aim of the review: Psoriasis is increasingly recognized as a systemic inflammatory disease frequently associated with a cluster of cardiometabolic comorbidities, including obesity, type 2 diabetes, and cardiovascular disease. Central to this association is the interleukin-17 (IL-17) signaling axis, a key driver of both cutaneous inflammation and systemic metabolic dysfunction. Materials and methods: This review examines the complex immunometabolic interactions mediated by IL-17 and synergistic cytokines such as TNF‑α, IL‑6, IL‑1β, IL‑23, and adipokines, which contribute to endothelial dysfunction, insulin resistance, and adipose-tissue inflammation. Results: Beyond its established role in psoriasis pathogenesis, the IL-17 pathway is implicated in the 'psoriatic march,' linking chronic skin inflammation to accelerated atherosclerosis. The advent of IL-17 inhibitors has transformed the management of moderate-to-severe psoriasis, achieving unprecedented skin clearance (PASI 90/100). Emerging evidence suggests that these agents may also exert potential beneficial effects on selected inflammatory and cardiometabolic markers. However, their direct impact on metabolic parameters remains under investigation. Conclusion: Understanding these shared molecular pathways is essential for adopting a holistic therapeutic approach that addresses both cutaneous disease and the systemic burden of psoriatic patients.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.



