Macrophage SBK2 suppresses inflammation and atherosclerosis by NLRP3 phosphorylation - PubMed
3 months ago
- #NLRP3
- #inflammation
- #atherosclerosis
- Macrophage SBK2 suppresses inflammation and atherosclerosis by phosphorylating NLRP3.
- SBK2 expression is elevated in advanced atherosclerotic plaques in both mice and humans.
- Genetic ablation or macrophage-specific SBK2 deficiency worsens plaque formation and inflammation.
- Macrophage-targeted SBK2 overexpression attenuates atherosclerosis progression.
- SBK2 phosphorylates NLRP3 at Ser161, leading to its autophagic degradation and inflammasome inactivation.
- Pharmacological activation of SBK2 with rebaudioside N (RN) reduces NLRP3-mediated inflammation and atherosclerotic burden.
- RN's therapeutic effects are abolished in SBK2-deficient models, confirming target specificity.
- SBK2 is identified as the sole known kinase mediating selective NLRP3 clearance.
- Targeting the SBK2-NLRP3 axis offers a precise therapeutic strategy for inflammatory cardiovascular risk.