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Tumor Necrosis Factor-Like Weak Inducer of Apoptosis (TWEAK)/Fibroblast Growth Factor-Inducible 14 (Fn14) Axis in

Nerea Méndez-Barbero1, Carmen Gutiérrez-Muñoz1, Rafael Blázquez-Serra1

  • 1Vascular Research Lab, IIS-Fundación Jiménez Díaz University Hospital, Av. Reyes Católicos 2, 28040 Madrid, Spain.

Cells
|February 15, 2020
PubMed

Insights

The tumor necrosis factor-like weak inducer of apoptosis (TWEAK) and its receptor fibroblast growth factor-inducible 14 (Fn14) axis drives pathological cardiovascular remodeling. Understanding this TWEAK/Fn14 axis is crucial for developing new treatments for cardiovascular diseases.

Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • Immunology

Background:

  • Cardiovascular diseases (CVD) are a major cause of death globally.
  • Pathological vascular remodeling, driven by inflammation, underlies various CVDs.
  • The tumor necrosis factor superfamily plays a role in CVD pathogenesis.

Purpose of the Study:

  • To review the role of the TWEAK/Fn14 axis in pathological cardiovascular remodeling.
  • To highlight cellular components and signaling pathways involved in TWEAK/Fn14-mediated CVD.
  • To explore the implications of TWEAK/Fn14 activation in heart and vessel remodeling.

Main Methods:

  • Literature review focusing on the TWEAK/Fn14 axis in cardiovascular remodeling.
  • Analysis of studies investigating cytokine and receptor interactions in CVD.
  • Synthesis of data on cellular functions and biological processes regulated by TWEAK/Fn14.

Main Results:

  • TWEAK and its receptor Fn14 are highly expressed during pathological cardiovascular remodeling.
  • The TWEAK/Fn14 axis regulates cellular proliferation, differentiation, apoptosis, inflammation, and fibrosis.
  • Persistent TWEAK/Fn14 activation is implicated in both acute and chronic CVD-related remodeling.

Conclusions:

  • The TWEAK/Fn14 axis is a significant contributor to pathological cardiovascular remodeling in CVD.
  • Targeting the TWEAK/Fn14 pathway may offer therapeutic strategies for cardiovascular diseases.
  • Further research into TWEAK/Fn14 signaling is warranted for CVD treatment development.

Keywords:
Fn14TWEAKheart failurestrokevascular remodeling

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