Targeting VDAC1-dependent mtDNA release attenuates fibroblast innate immune activation and vitiligo pathogenesis - PubMed
4 hours ago
- #Oxidative Stress
- #Vitiligo
- #Fibroblasts
- Vitiligo is a chronic depigmentary disorder initiated by oxidative stress, leading to melanocyte destruction.
- Dermal fibroblasts play a key role in vitiligo pathogenesis by releasing mitochondrial DNA (mtDNA) under oxidative stress.
- Oxidative stress in normal human dermal fibroblasts (NHDFs) induces VDAC1-dependent mtDNA release without apoptosis.
- Released mtDNA activates the cGAS-STING pathway and NLRP3 inflammasome, driving inflammatory cytokine expression.
- Pharmacological inhibition of VDAC1 oligomerization with VBIT-4 prevents mtDNA leakage and attenuates inflammation.
- Targeting VDAC1-mtDNA-cGAS-STING axis in fibroblasts shows promise for vitiligo treatment.