The cGAS-STING pathway contributes to cisplatin-induced skeletal muscle atrophy through altered proteostasis and myogenic signaling - PubMed
6 hours ago
- #Skeletal muscle
- #Chemotherapy-induced atrophy
- #cGAS-STING pathway
- The cGAS-STING pathway is implicated in cisplatin-induced skeletal muscle atrophy.
- Pharmacological activation of STING with DMXAA worsened cisplatin-induced muscle atrophy.
- Genetic deletion of cGAS or STING attenuated cisplatin-induced muscle atrophy in mice.
- Muscle-specific cGAS knockout preserved muscle weight and fiber diameter after cisplatin treatment.
- RNA sequencing revealed altered inflammatory signaling, proteasome function, and autophagy pathways.
- Reduced expression of atrophy genes (FBXO32, Murf1) and preserved myogenic regulators in cGAS-deficient mice.
- NF-κB signaling and interferon-stimulated gene expression were diminished.
- Targeting the cGAS-STING pathway may be a therapeutic strategy to prevent chemotherapy-induced muscle atrophy.