PPAR-γ suppresses macrophage senescence and allergic airway inflammation through controlling lipid metabolic pathways - PubMed
3 hours ago
- #Allergic Asthma
- #PPAR-γ
- #Macrophage Senescence
- PPAR-γ suppresses macrophage senescence and allergic airway inflammation by regulating lipid metabolic pathways.
- Cellular senescence contributes to chronic lung diseases, with PPAR-γ playing a regulatory role in multiple cell types.
- Single-cell RNA sequencing (scRNA-seq) in an allergic asthma mouse model showed enhanced senescence in mononuclear phagocytes (MNPs).
- Elimination of senescent cells reduced airway inflammation and Th2 cytokine levels (IL-4, IL-5).
- Macrophage-specific PPAR-γ deletion (PpargΔCD11c) worsened airway inflammation and increased cellular senescence.
- Rosiglitazone reduced allergen-induced senescence and proinflammatory mediators in alveolar macrophages.
- Inhaled phosphatidylserine-modified liposomes (PSL-ROSI) effectively delivered rosiglitazone to lung macrophages, bypassing the airway mucus barrier.
- PPAR-γ promotes macrophage lipid metabolic programs (e.g., CD36, Fabp4), highlighting its therapeutic potential for asthma.