Key result
Myeloid NCOR1 deletion aggravates atherosclerosis and accelerates foam cell formation via enhanced PPARγ signaling.
Why the study?
The role of nuclear receptor corepressors, specifically macrophage NCOR1, in atherogenesis was unknown despite evidence that Ncor1 deletion increases atherosclerotic molecule expression in macrophages.
Population
Myeloid cell-specific Ncor1 knockout mice crossbred with Ldlr knockouts and human atherosclerotic plaques
Comparison
Myeloid cell-specific deletion of NCOR1 vs control mice with intact NCOR1
Design
Preclinical study using genetically modified mice and human plaque analysis
Authors
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No implications for current clinical practice; leaves open therapeutic potential of macrophage NCOR1 in human atherosclerosis.
Macrophage NCOR1 protects against atherosclerosis by repressing pro-atherogenic PPARγ target genes, suggesting that stabilizing NCOR1-PPARγ binding could be a potential therapeutic strategy to block lesion progression.
Oppi et al. (2019) studied Atherosclerosis. Macrophage Ncor1-deficiency vs. Wild-type / NCOR1 presence was evaluated on Atherosclerosis development and plaque characteristics. Myeloid cell-specific deletion of NCOR1 aggravates atherosclerosis development and increases foam cell formation by enhancing pro-atherogenic PPARγ target gene expression.