Nuclear receptor Dax1 promotes atherosclerosis by lipid transport inhibition and autophagy suppression in macrophages
Authors' conclusion
This study demonstrates that Dax1 levels are increased in atherosclerotic plaques. Dax1 promotes atherosclerosis by interacting with TFEB to suppress autophagy and inhibiting LXRα for lipid transport in macrophage
Study context
- Population
- Human atherosclerotic arteries and atherosclerosis mouse models
- Comparison
- Macrophage Dax1 knockout/knockdown vs controls
Main finding
As reported in the abstract
- Dax1 mRNA up-regulated among nuclear receptors (NRs) in atherosclerotic vs non-atherosclerotic arteries, prominently in macrophages
- Macrophage-specific Dax1 knockout mice had less atherosclerosis than controls
- Dax1 inhibited LXRα and interacted directly with transcription factor EB (TFEB) to suppress autophagy, causing lipid accumulation and inflammation in macrophages
- 2'-Deoxycytidine concentration dependently decreased Dax1, enhanced autophagy, reduced lipid accumulation and inhibited atherosclerosis in mice
Original publication
Nuclear receptor Dax1 promotes atherosclerosis by lipid transport inhibition and autophagy suppression in macrophages. Eur Heart J. Published 22 April 2025. doi:10.
Summarised from the published abstract; every number is checked against it