Tumor necrosis factor-like weak inducer of apoptosis (TWEAK) and kidney disease

Marta Ruiz-Ortega1, Alberto Ortiz, Adrian M Ramos

  • 1aIIS-Fundación Jiménez Díaz bREDinREN cUniversidad Autonoma de Madrid dIRSIN, Madrid, Spain.

Abstract

Insights

Targeting the tumor necrosis factor-like weak inducer of apoptosis (TWEAK) shows promise for treating kidney injury. TWEAK targeting is well-tolerated in humans and may offer new therapies for various kidney diseases.

Area of Science:

  • Nephrology
  • Immunology
  • Molecular Biology

Background:

  • The cytokine tumor necrosis factor-like weak inducer of apoptosis (TWEAK) is implicated in kidney injury.
  • TWEAK has potential as a biomarker in kidney disease.
  • Previous studies linked TWEAK to kidney injury in animal models.

Purpose of the Study:

  • To review recent findings on TWEAK's role in kidney injury.
  • To explore the therapeutic potential of TWEAK targeting in kidney diseases.
  • To summarize the clinical progress of TWEAK inhibition.

Main Methods:

  • Review of experimental studies on TWEAK in kidney injury.
  • Analysis of recent research identifying TWEAK targets in renal cells.
  • Evaluation of clinical trial data for TWEAK inhibitors.

Main Results:

  • TWEAK promotes tubular cell injury and kidney inflammation.
  • TWEAK upregulates CXCL16 and downregulates Klotho in tubular cells.
  • TWEAK inhibition reduced kidney fibrosis in various injury models.
  • TWEAK may link chronic kidney disease and cancer.
  • TWEAK targeting is well-tolerated in a Phase I clinical trial.

Conclusions:

  • TWEAK targeting demonstrates clinical potential for immune and non-immune kidney injuries.
  • Further clinical trials are investigating TWEAK inhibition for lupus nephritis.
  • Novel therapeutic strategies targeting TWEAK are emerging for kidney disease.

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