Macrophage NCOR1 protects from atherosclerosis by repressing a pro-atherogenic PPARγ signature
Authors' conclusion
Our findings show that macrophage NCOR1 blocks the pro-atherogenic functions of PPARγ in atherosclerosis
Study context
- Population
- Low-density lipoprotein receptor (Ldlr) knockout mice; mouse and human macrophages; human carotid atherosclerotic plaques
- Comparison
- Myeloid cell-specific Ncor1 deletion vs NCOR1-intact macrophages
Methodological detailsmyeloid cell-specific Ncor1 knockout mice crossbred with Ldlr knockouts
- Myeloid cell-specific Ncor1 knockout mice crossbred with Ldlr knockouts
Main finding
As reported in the abstract
- Myeloid NCOR1 deletion aggravates atherosclerosis development in mice
- Macrophage Ncor1-deficiency: increased foam cell formation, enhanced pro-inflammatory cytokine expression
- Lesions with larger necrotic cores and thinner fibrous caps
- Effects mediated via suppression of PPARγ target genes; without NCOR1, enhanced CD36 expression and increased oxidized LDL uptake
- Human plaques: NCOR1 expression reduced, PPARγ signature increased; more pronounced in ruptured vs non-ruptured carotid plaques
Original publication
Macrophage NCOR1 protects from atherosclerosis by repressing a pro-atherogenic PPARγ signature. Eur Heart J. Published 16 September 2019. doi:10.
Summarised from the published abstract; every number is checked against it