cGAS-STING signaling pathway promotes ischemic kidney injury by regulating HK3-mediated lipid accumulation - PubMed
3 hours ago
- #Lipid Metabolism
- #cGAS-STING
- #Kidney Fibrosis
- The cGAS-STING signaling pathway is upregulated in fibrotic kidneys from CKD patients and mice with ischemia-reperfusion injury (IRI).
- Genetic or pharmacological inhibition of STING reduces renal fibrosis, inflammation, and lipid accumulation in IRI mice, linked to HK3-mediated lipid metabolism.
- STING inhibition suppresses NF-κB activation, reducing HK3 upregulation and attenuating fibrosis, inflammation, and lipid accumulation in renal cells.
- The cGAS-STING pathway promotes NF-κB p65 binding to the HK3 promoter, leading to HK3 upregulation, dysregulated lipid metabolism, and renal fibrosis.
- The cGAS-STING-NF-κB-HK3 axis is a potential therapeutic target for early-stage renal fibrosis.