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Updated: Jun 14, 2026
12:04
The bm12 Inducible Model of Systemic Lupus Erythematosus (SLE) in C57BL/6 Mice
Published on: November 1, 2015
TWEAK as a target for therapy in systemic lupus erythematosus
Rui-Xue Leng1, Hai-Feng Pan, Wei-Zi Qin
1Department of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University, 81 Meishan Road, 230032, Hefei, Anhui, People's Republic of China.
Molecular Biology Reports
|April 2, 2010
Summary
Tumor necrosis factor (TNF)-like weak inducer of apoptosis (TWEAK) and its receptor Fn14 are involved in inflammation and cell death. Targeting this pathway may offer new therapies for systemic lupus erythematosus (SLE).
Area of Science:
- Immunology
- Cell Biology
- Rheumatology
Background:
- Tumor necrosis factor (TNF)-like weak inducer of apoptosis (TWEAK) is a proinflammatory cytokine.
- TWEAK signals through the fibroblast growth factor-inducible 14 (Fn14) receptor.
- The TWEAK-Fn14 pathway regulates cell proliferation, death, and inflammation.
Purpose of the Study:
- To review the role of the TWEAK-Fn14 pathway in systemic lupus erythematosus (SLE).
- To discuss the therapeutic potential of modulating the TWEAK-Fn14 pathway in SLE.
Main Methods:
- Literature review of studies on TWEAK, Fn14, and SLE.
- Analysis of the TWEAK-Fn14 pathway's involvement in SLE pathogenesis.
- Evaluation of potential therapeutic strategies targeting this pathway.
Main Results:
- TWEAK-Fn14 pathway activation is implicated in renal, vascular, and neurological complications.
- These complications are frequently observed in SLE patients.
- Modulating the TWEAK-Fn14 pathway shows promise for SLE treatment.
Conclusions:
- The TWEAK-Fn14 pathway is a potential contributor to SLE pathogenesis.
- Targeting the TWEAK-Fn14 pathway represents a promising therapeutic avenue for SLE.
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