Psoriasis and increased cardiovascular risk: cutaneous inflammation as a systemic marker-the role of IL-17 and endothelial dysfunction

Psoriasis, a chronic immune-mediated inflammatory dermatosis, has been increasingly recognized as a systemic condition associated with elevated cardiovascular risk. Emerging evidence suggests that the persistent inflammatory state in psoriasis, driven by key cytokines such as interleukin-17 (IL-17), contributes to endothelial dysfunction and accelerated atherosclerosis, thereby predisposing affected individuals to major adverse cardiovascular events. This article explores the pathophysiological mechanisms linking cutaneous inflammation to systemic vascular impairment, with a particular focus on the role of IL-17 in promoting endothelial activation, leukocyte recruitment and plaque instability. Furthermore, we discuss the clinical implications of psoriasis as an independent risk factor for cardiovascular disease, emphasizing the importance of multidisciplinary management strategies to mitigate long-term cardiovascular morbidity in this patient population.