TWEAK as a target for therapy in systemic lupus erythematosus.

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.

• Authors: Rui-Xue Leng, Hai-Feng Pan, Wei-Zi Qin, Chao Wang, Li-Li Chen, Jin-Hui Tao, Dong-Qing Ye
• Journal: Molecular biology reports (Mol Biol Rep) Vol. 38 Issue 1 Pg. 587-92 (Jan 2011) ISSN: 1573-4978 [Electronic] Netherlands
• PMID: 20358293 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)

Chemical References

• Cytokine TWEAK
• Receptors, Tumor Necrosis Factor
• TNFRSF12A protein, human
• TNFSF12 protein, human
• TWEAK Receptor
• Tumor Necrosis Factors

Topics

• Cytokine TWEAK
• Humans
• Lupus Erythematosus, Systemic (etiology, pathology, therapy)
• Receptors, Tumor Necrosis Factor (metabolism)
• TWEAK Receptor
• Tumor Necrosis Factors (metabolism)