Key result
VSMC-specific Lmod1 loss triggers rapid, diffuse, occlusive coronary atherosclerosis under atherogenic conditions in mice.
Why the study?
LMOD1 is a coronary artery disease risk gene, but its role in coronary artery pathophysiology remains unknown.
Does the loss of LMOD1 in vascular smooth muscle cells trigger coronary atherosclerosis in atherogenic mouse models?
Does the loss of LMOD1 in vascular smooth muscle cells trigger coronary atherosclerosis in atherogenic mouse models?
VSMC-specific loss of the CAD risk gene LMOD1 triggers rapid and severe coronary atherosclerosis in mice, establishing its critical role in maintaining coronary homeostasis.
Captured external expert commentary on this paper, strongest first. Original sources are linked where available.
“Our findings suggest that LMOD1 functions as an important artery-protective gene. When this protective mechanism is lost, coronary arteries become highly susceptible to rapid cholesterol-driven plaque buildup.”
VSMC Lmod1 loss drives murine coronary atherosclerosis; leaves open whether LMOD1 variants contribute to human CAD.
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Salem et al. (2026) studied Coronary atherosclerosis (n=500). VSMC-restricted Lmod1 knockout (Lmod1 SMKO) vs. Lmod1 WT control mice was evaluated on Development of coronary atherosclerosis. VSMC-restricted loss of Lmod1 triggered rapid-onset, diffuse, occlusive coronary atherosclerosis under atherogenic conditions, whereas control mice developed no such disease.
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