Particle.news

Download on the App Store

Silenced Liver Clock Gene Drives Cancer Cachexia, Reveals New Therapeutic Targets

Reactivating REV-ERBα in mouse models curbs muscle and fat wasting, with patient hepatokine profiles pointing to biomarker potential

Image

Overview

  • Researchers discovered that cancer cachexia silences the liver’s circadian regulator REV-ERBα, reprogramming metabolic pathways
  • Loss of REV-ERBα triggers hepatic secretion of hepatokines LBP, ITIH3 and IGFBP1, which drive muscle and fat degradation in cell and animal models
  • Liver-targeted reactivation of REV-ERBα in mice significantly reduced body mass loss and preserved muscle and adipose tissue
  • Preclinical inhibition of the identified hepatokines effectively mitigated tissue wasting in muscle and fat models
  • Patient blood analyses revealed elevated hepatokine levels in cachectic cancer patients, indicating new avenues for early diagnosis