银屑病与代谢综合征(MS)相关且心血管事件多发，严重影响银屑病的病情和转归，但机制不清。C1q-TNF-related protein-3(CTRP3)是一种具有调控代谢、炎症抵抗和心血管保护作用的新因子。我们发现银屑病患者CTRP3水平显著低于正常人，且银屑病效应分子TNF-α可下调其表达，CTRP3又与患者瘦素、脂联素水平相关。因此我们提出CTRP3可能是银屑病与代谢综合征的重要联系分子，一方面通过影响代谢使银屑病患者易患MS；另一方面使T细胞等产生更多的炎症因子，加重银屑病病情，形成一个银屑病与MS互为因果的恶性循环。本课题拟在明确CTRP3与银屑病相关的基础上，在体外实验和动物实验中分别研究1. 银屑病炎症因子对CTRP3表达及MS发生的影响；2. CTRP3对银屑病炎症发生发展的影响。深入探讨银屑病患者CTRP3水平和功能低下的机制，阐明CTRP3在银屑病患者发生MS中的意义。

Epidemiological studies suggest that patients with psoriasis are not only burdened with its symptoms, but also have an increased prevalence of metabolic disorders, including metabolic syndrome(MS)and cardiovascular comorbidities. It is believed that MS has significantly risk effect on severity and manifestations of psoriasis, but the molecular linker between these two diseases is not clear. C1q-TNF-related protein-3(CTRP3), a very important type of C1q family adipokines which modulate metabolic and immune response, has anti-inflammatory and cardiovascular protection functions. We hypothesis that CTRP3 serves as a molecular linker among psoriasis, metabolic disorders and cardiovascular comorbidities based on our pre-investigations of abnormal decreased CTRP3 levels in psoriasis patients compared to normal controls. To elucidate the pathogenic functions of CTRP3 in psoriasis, we will study the melocular mechanism of CTRP3 expression and the metabolic-regulated functions in vitro and in vivo. We also will investigate the anti-inflammatory functions in the homeostasis of the micro-immuno-environment of psoriasis patients. Our research reveals the function of CTRP3 in psoriasis pathogenesis and opens a new area of adiopkines of psoriasis treatment strategies.