Role of KLF4 in Neutrophil Aging in Periodontitis with Metabolic Syndrome - PubMed
5 hours ago
- #neutrophil aging
- #metabolic syndrome
- #periodontitis
- Metabolic syndrome (MetS) and periodontitis (PD) are interconnected health burdens with unclear inflammatory interplay.
- MetS enhances infiltration of senescent neutrophils into periodontal tissues, exhibiting a proinflammatory phenotype.
- Senescent neutrophils show increased secretion of inflammatory factors, enhanced neutrophil extracellular traps (NETs), and glycolytic metabolic shift.
- KLF4 is downregulated in comorbid MetS and PD, playing a key role in neutrophil aging.
- Adoptive transfer of MetS-derived or Klf4-deficient neutrophils worsens periodontal inflammation and bone destruction.
- KLF4 knockdown in neutrophil-like cells promotes metabolic reprogramming and proinflammatory responses.
- Rosiglitazone stabilizes KLF4, alleviating periodontal damage and improving insulin resistance in mice.
- Therapeutic effects of rosiglitazone are abolished in Klf4-deficient models, confirming KLF4's critical role.
- KLF4 activation is a promising therapeutic strategy for mitigating MetS-exacerbated periodontitis.