Macrophage SBK2 suppresses inflammation and atherosclerosis by NLRP3 phosphorylation
Authors' conclusion
Macrophage SBK2 serves as an endogenous safeguard factor that suppresses atherosclerosis by phosphorylating NLRP3 to enable its selective autophagic degradation.
Study context
- Population
- Murine models of atherosclerosis (high-fat diet) and human atherosclerotic lesions
- Comparison
- SBK2 deficiency or overexpression, and SBK2 activation with rebaudioside N, in atherosclerosis
Methodological detailsmurine models, human atherosclerotic lesions, single-cell sequencing, small-molecule library screening
- Murine models
- Human atherosclerotic lesions
- Single-cell sequencing
- Small-molecule library screening
Main finding
As reported in the abstract
- SBK2 expression elevated in macrophages within advanced murine and human atherosclerotic plaques
- Whole-body or macrophage-specific SBK2 deficiency exacerbated plaque formation and inflammatory responses
- Macrophage-targeted SBK2 overexpression attenuated disease progression
- SBK2 phosphorylates NLRP3 at Ser161, triggering Tollip-dependent autophagic degradation and inflammasome inactivation
- Rebaudioside N (RN) suppressed NLRP3-mediated IL-1β/IL-18 secretion, reduced inflammation and atherosclerotic burden
- RN's effects completely abolished in SBK2-deficient models
Original publication
Macrophage SBK2 suppresses inflammation and atherosclerosis by NLRP3 phosphorylation. Eur Heart J. Published 13 February 2026. doi:10.
Composed by AI from the published abstract and checked against it. How Briefs are made →