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TWEAK/Fn14 Activation Participates in Skin Inflammation
Qilu Liu1, Shengxiang Xiao1, Yumin Xia1
1Department of Dermatology, The Second Affiliated Hospital, School of Medicine, Xi'an Jiaotong University, Xi'an, China.
Mediators of Inflammation
|October 18, 2017
Summary
The TWEAK/Fn14 pathway regulates skin inflammation and cell fate. Dysregulation contributes to various skin diseases, suggesting it as a therapeutic target.
Area of Science:
- Dermatology and immunology, focusing on molecular pathways in skin diseases.
Background:
- Tumor necrosis factor- (TNF-) like weak inducer of apoptosis (TWEAK) interacts with its receptor, fibroblast growth factor-inducible 14 (Fn14).
- The TWEAK/Fn14 pathway is implicated in skin inflammation, modulating keratinocyte responses via nuclear factor-κB (NF-κB) signaling and cytokine production.
Purpose of the Study:
- To elucidate the role of the TWEAK/Fn14 signaling pathway in the pathogenesis of skin disorders.
- To explore the TWEAK/Fn14 pathway as a potential therapeutic target for inflammatory skin diseases.
Main Methods:
- Review of literature on TWEAK/Fn14 signaling in skin biology and disease.
- Analysis of the molecular mechanisms involving TWEAK/Fn14 in keratinocyte function and inflammatory responses.
Main Results:
- TWEAK/Fn14 activation influences cytokine production (interleukins, MCP-1, RANTES, IP-10) and keratinocyte cell fate.
- While transient activation aids tissue repair, persistent activation leads to inflammatory infiltration and damage.
- The pathway is critically involved in the pathogenesis of psoriasis, atopic dermatitis, vasculitis, HPV-related conditions, and autoimmune skin diseases.
Conclusions:
- The TWEAK/Fn14 pathway is a key player in various skin inflammatory conditions.
- Targeting the TWEAK/Fn14 pathway offers a promising strategy for developing new treatments for skin inflammatory diseases.
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