Role of tumor necrosis factor-like weak inducer of apoptosis (TWEAK)/fibroblast growth factor-inducible 14 (Fn14) axis in rheumatic diseases.
- Author:
Li-Xiu ZHU
1
;
Hai-Hong ZHANG
;
Yi-Fang MEI
;
Yan-Ping ZHAO
;
Zhi-Yi ZHANG
Author Information
1. Department of Rheumatology, First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, China.
- Publication Type:Journal Article
- MeSH:
Arthritis, Rheumatoid;
etiology;
Cytokine TWEAK;
Humans;
Lupus Erythematosus, Systemic;
etiology;
Receptors, Tumor Necrosis Factor;
physiology;
Rheumatic Diseases;
etiology;
Scleroderma, Systemic;
etiology;
TWEAK Receptor;
Tumor Necrosis Factors;
physiology
- From:
Chinese Medical Journal
2012;125(21):3898-3904
- CountryChina
- Language:English
-
Abstract:
Tumor necrosis factor (TNF)-like weak inducer of apoptosis (TWEAK) is a member of the TNF superfamily of structurally related cytokines and is known to induce proliferation, migration, differentiation, apoptotic cell death, inflammation, and angiogenesis. These physiological processes are induced by the binding of TWEAK to fibroblast growth factor-inducible 14 (Fn14), a highly inducible cell-surface receptor that is linked to several intracellular signaling pathways, including the nuclear factor-κB (NF-κB) pathway. This review discusses the role of the TWEAK-Fn14 axis in several rheumatic diseases and the potential therapeutic benefits of modulation of the TWEAK-Fn14 pathway.
