Tissue-resident macrophage survival depends on mitochondrial function regulated by SerpinB2 in chronic inflammation - PubMed
8 days ago
- #inflammation
- #mitochondria
- #macrophage
- Tissue-resident macrophage survival in chronic inflammation depends on mitochondrial function regulated by SerpinB2.
- Visceral adipose tissue (VAT)-resident macrophages are enriched with mitochondrial-specific antioxidant enzymes, promoting VAT homeostasis and insulin sensitivity.
- SerpinB2 promotes adipose resident macrophage survival by regulating mitochondrial oxidative phosphorylation and preventing cytochrome c release via glutathione production.
- Chronic inflammation, such as obesity, reduces SerpinB2 expression in VAT macrophages, leading to their decline.
- Interferon-γ elevation in diabetes induces Ikaros, which suppresses SerpinB2 expression by binding to its promoter.
- Restoring SerpinB2 expression or supplementing with N-acetylcysteine improves VAT resident macrophage survival, reduces adipocyte size, and enhances glucose tolerance and insulin sensitivity.