AI Summary: This study identifies a single gene, LMOD1, as a 'gatekeeper' for heart health. By removing this gene from the smooth muscle cells of mouse arteries, researchers found that the mice developed severe heart disease (atherosclerosis) almost immediately—even when eating healthy.
Coronary artery disease (CAD) remains a leading cause of mortality, yet the mechanisms by which specific risk genes contribute to atherosclerosis are often unclear. We investigate the role of *Leiomodin1* (LMOD1), a gene highly associated with CAD risk in human GWAS. Using a novel smooth muscle-specific knockout mouse model, we demonstrate that loss of LMOD1 leads to rapid-onset coronary atherosclerosis, even on a normal diet. We identify LMOD1 as a critical regulator of smooth muscle cell 'phenotypic switching', where its absence causes cells to lose their contractile identity and become pro-inflammatory. This study identifies LMOD1 as a major 'gatekeeper' of coronary health and a potential target for therapeutic intervention.
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