Molecular Biology Reports

, Volume 38, Issue 1, pp 587–592

TWEAK as a target for therapy in systemic lupus erythematosus

  • Rui-Xue Leng
  • Hai-Feng Pan
  • Wei-Zi Qin
  • Chao Wang
  • Li-Li Chen
  • Jin-Hui Tao
  • Dong-Qing Ye
Article

DOI: 10.1007/s11033-010-0144-9

Cite this article as:
Leng, RX., Pan, HF., Qin, WZ. et al. Mol Biol Rep (2011) 38: 587. doi:10.1007/s11033-010-0144-9

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.

Keywords

TWEAKFn14Systemic lupus erythematosus

Copyright information

© Springer Science+Business Media B.V. 2010

Authors and Affiliations

  • Rui-Xue Leng
    • 1
  • Hai-Feng Pan
    • 1
  • Wei-Zi Qin
    • 1
  • Chao Wang
    • 1
  • Li-Li Chen
    • 1
  • Jin-Hui Tao
    • 2
  • Dong-Qing Ye
    • 1
  1. 1.Department of Epidemiology and Biostatistics, School of Public HealthAnhui Medical UniversityHefeiPeople’s Republic of China
  2. 2.Department of RheumatologyAnhui Provincial Hospital affiliated to Anhui Medical UniversityHefeiPeople’s Republic of China