LDHB K156 lactylation links cGAS-STING-mediated metabolic reprogramming to NLRP3 inflammasome activation in sepsis-associated acute kidney injury - PubMed
2 days ago
- #NLRP3 inflammasome
- #SA-AKI
- #LDHB K156 lactylation
- The study explores the role of LDHB K156 lactylation in sepsis-associated acute kidney injury (SA-AKI).
- Sepsis induces glycolysis, lactate accumulation, and NLRP3 inflammasome activation.
- Lactyl-proteomics identified significant upregulation of LDHB lysine 156 (K156) lactylation.
- cGAS-STING signaling promotes glycolytic reprogramming and lactate production, facilitating LDHB K156 lactylation.
- LDHB WT exacerbates renal dysfunction and inflammasome activation compared to the K156R mutant.
- Targeting the LDHB K156 lactylation regulatory axis could offer a therapeutic strategy for SA-AKI.