银屑病
促炎细胞因子
贾纳斯激酶
蛋白激酶B
发病机制
医学
PI3K/AKT/mTOR通路
免疫学
信号转导
人口
癌症研究
生物
细胞因子
炎症
细胞生物学
环境卫生
作者
Lulu Xia,Hongxin Li,Long Li,Wei Ruan,Jiajia Ma,Shan Xu,Dan Qiao
标识
DOI:10.1002/ardp.202400621
摘要
Psoriasis is a prevalent chronic systemic immune disease characterized by T-cellmediated hyperproliferation of keratinized cells. Among its various manifestations, plaque-type psoriasis is the most common. Treatment options for psoriasis encompass topical medications, biological therapies, phototherapy techniques, and others. However, traditional treatments are associated with numerous side effects. In contrast, targeted therapy has garnered increasing attention due to its high selectivity, strong safety profile, and favorable therapeutic outcomes. Patients with psoriasis lesions exhibit elevated levels of proinflammatory cytokines compared with the general population. These proinflammatory cytokines have been implicated in mediating psoriasis pathogenesis by inducing keratinocyte proliferation through multiple signaling pathways within the body. This study will delve into the Janus kinase-signal transducers and activators of transcription, phosphatidylinositol 3 kinase (PI3K)-protein kinase B (PKB, also known as AKT), and nuclear factor Kappa-light-chain-enhancer of activated B cells signaling pathways to elucidate their roles in mediating psoriasis pathogenesis. In addition, we will summarize potential targets relevant to the treatment of psoriasis and discuss the design and activity assessment of their inhibitors. It also provides new insights for further in-depth study of psoriasis and development of novel molecularly targeted inhibitors.
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