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TWEAK as a target for therapy in systemic lupus erythematosus
Authors:Rui-Xue?Leng  Hai-Feng?Pan  Wei-Zi?Qin  Chao?Wang  Li-Li?Chen  Jin-Hui?Tao  Email author" target="_blank">Dong-Qing?YeEmail author
Institution:(1) Department of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University, 81 Meishan Road, 230032 Hefei, Anhui, People’s Republic of China;(2) Department of Rheumatology, Anhui Provincial Hospital affiliated to Anhui Medical University, 17 Lujiang Road, 230001 Hefei, Anhui, People’s Republic of China;
Abstract:Tumor necrosis factor (TNF)-like weak inducer of apoptosis (TWEAK) is a recently identified proinflammatory cytokine of the TNF superfamily. Through activation of the fibroblast growth factor-inducible 14 (Fn14) receptor, TWEAK regulates cell proliferation, cell death and inflammation. The available evidences have indicated that TWEAK might be a target for therapeutic intervention in renal, vascular injury and neuropathy. Since renal, vascular and neuropsychiatric complications are frequently encountered in systemic lupus erythematosus (SLE)—a systemic autoimmune disease, TWEAK-Fn14 pathway may be implicated in the pathogenesis of SLE. In this review, we will discuss the TWEAK-Fn14 pathway and the therapeutic potential of modulating this pathway in SLE.
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