TWEAK/Fn14 axis in respiratory diseases

Clin Chim Acta. 2020 Oct:509:139-148. doi: 10.1016/j.cca.2020.06.007. Epub 2020 Jun 8.

Abstract

Tumor necrosis factor-like weak inducer of apoptosis (TWEAK) is a well known multifunctional cytokine extensively distributed in cell types and tissues. Accumulating evidence has shown that TWEAK binding to the receptor factor-inducible 14 (Fn14) participates in diverse pathologic processes including cell proliferation and death, angiogenesis, carcinogenesis and inflammation. Interestingly, alterations of intracellular signaling cascades are correlated to the development of respiratory disease. Recently, a several lines of evidence suggests that TWEAK in lung tissues are closely associated with these signaling pathways. In this review, we explore if TWEAK could provide a novel therapeutic strategy for managing respiratory disease in general and pulmonary arterial hypertension (PAH), obstructive sleep apnea syndrome (OSAS), asthma, idiopathic pulmonary fibrosis (IPF), chronic obstructive pulmonary disease (COPD) and non-small cell lung cancer (NSCLC), specifically.

Keywords: Fn14; Respiratory diseases; TWEAK.

Publication types

  • Review

MeSH terms

  • Carcinoma, Non-Small-Cell Lung*
  • Cytokine TWEAK
  • Humans
  • Lung Neoplasms*
  • Receptors, Tumor Necrosis Factor
  • TWEAK Receptor / genetics
  • Tumor Necrosis Factors

Substances

  • Cytokine TWEAK
  • Receptors, Tumor Necrosis Factor
  • TNFRSF12A protein, human
  • TNFSF12 protein, human
  • TWEAK Receptor
  • Tumor Necrosis Factors