TWEAK/Fn14 axis in respiratory diseases

Min Wang1, Zhijuan Xie2, Jin Xu3

  • 1Department of Otorhinolaryngology, University of South China Affiliated Nanhua Hospital, Hengyang 421002, China.

Insights

Tumor necrosis factor-like weak inducer of apoptosis (TWEAK) shows potential in treating lung diseases. This review explores TWEAK

Area of Science:

  • Immunology
  • Cell Biology
  • Pulmonology

Background:

  • Tumor necrosis factor-like weak inducer of apoptosis (TWEAK) is a cytokine involved in various pathological processes.
  • TWEAK interacts with its receptor, factor-inducible 14 (Fn14).
  • Aberrant intracellular signaling pathways are linked to respiratory diseases.

Purpose of the Study:

  • To review the role of TWEAK in lung tissues.
  • To explore TWEAK as a potential therapeutic strategy for respiratory diseases.

Main Methods:

  • Literature review of TWEAK's involvement in cellular processes.
  • Analysis of TWEAK's association with signaling pathways in lung tissues.
  • Examination of TWEAK's potential in specific respiratory conditions.

Main Results:

  • TWEAK participates in cell proliferation, death, angiogenesis, carcinogenesis, and inflammation.
  • Evidence suggests TWEAK is closely associated with signaling pathways in lung tissues.
  • TWEAK's role in pulmonary arterial hypertension, obstructive sleep apnea syndrome, asthma, idiopathic pulmonary fibrosis, chronic obstructive pulmonary disease, and non-small cell lung cancer is under investigation.

Conclusions:

  • TWEAK is a multifunctional cytokine with implications in diverse pathologies.
  • Alterations in intracellular signaling are connected to respiratory disease development.
  • TWEAK presents a potential novel therapeutic avenue for managing a range of respiratory diseases.

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