牛皮癣是一种慢性免疫介导疾病，影响全球超过 2-3% 的人口，严重影响生活质量。尽管有各种治疗干预措施，但人们仍然担心病变复发和免疫监视的潜在改变会促进癌症进展。在了解细胞和分子途径方面的最新进展揭示了银屑病病因学的关键因素，包括 IL-17、22、23、TNF-α、PDE-4、JAK-STAT 抑制剂和 AhR 激动剂。这项工作探讨了 S 期激酶相关蛋白 2 (Skp2) 作为银屑病治疗靶点的潜力。这篇综述涵盖了目前对银屑病病理生理学的理解，包括免疫失调以及角质形成细胞和泛素的作用。它还深入研究了 Skp2 在细胞周期调节中的作用，及其与银屑病中血管生成和泛素的相关性。还讨论了针对 Skp2 的不断发展的治疗方法，包括小分子抑制剂。针对 Skp2 有望开发新的银屑病治疗方法。通过调节 Skp2 活性或表达，有可能干预疾病背后的炎症和增殖过程。有必要对 Skp2 抑制剂及其在临床前和临床环境中的功效进行进一步研究，以充分发挥 Skp2 作为银屑病治疗靶点的潜力。

Psoriasis is a chronic immune-mediated disorder affecting over 2-3% of the population worldwide, significantly impacting quality of life. Despite the availability of various therapeutic interventions, concerns persist regarding lesion recurrence and potential alterations in immune surveillance promoting cancer progression. Recent advancements in understanding cellular and molecular pathways have unveiled key factors in psoriasis etiology, including IL-17, 22, 23, TNF-α, PDE-4, JAK-STAT inhibitors, and AhR agonists. This work explores the potential of S-phase kinase-associated protein 2 (Skp2) as a therapeutic target in psoriasis.This review covers the current understanding of psoriasis pathophysiology, including immune dysregulation, and the role of keratinocytes and ubiquitin. It also delves into Skp2 role in cell cycle regulation, and its correlation with angiogenesis and ubiquitin in psoriasis. The evolving therapeutic approaches targeting Skp2, including small molecule inhibitors, are also discussed.Targeting Skp2 holds promise for developing novel therapeutic approaches for psoriasis. By modulating Skp2 activity or expression, it may be possible to intervene in inflammatory and proliferative processes underlying the disease. Further research into Skp2 inhibitors and their efficacy in preclinical and clinical settings is warranted to harness the full potential of Skp2 as a therapeutic target in psoriasis management.