ArticleClinical and translational medicine2026
Conditional knockout of membrane-type I matrix metalloproteinase in smooth muscle cells of adult mice alleviates atherosclerosis without affecting basic cardiovascular function.
Article in Clinical and translational medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Cell-Surface Signatures and Targets of Modulated Vascular Smooth Muscle Cells in Atherosclerosis: From State Identification to Precision Intervention.Journal of cardiovascular development and disease · 2026Review
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Authors and funding
16 authors.
Funding
Abstract
backgroundAtherosclerotic cardiovascular disease (ASCVD) is the leading cause of morbidity and mortality worldwide. Despite effective lipid-lowering treatments, substantial residual risks remain. In atherosclerosis, vascular smooth muscle cells (SMCs) undergo dedifferentiation, promoting disease progression. Membrane-type I matrix metalloproteinase (MT1-MMP/MMP14) promotes SMC dedifferentiation. However, the effect of inhibiting MMP14 in adults, particularly those with existing atherosclerotic plaques, is unclear.
methodsWe developed an inducible conditional SMC-specific MMP14 knockout mouse model. Cardiac and vascular function were assessed using echocardiography and wire myography, respectively. Atherosclerosis progression and regression were evaluated in Ldlr
resultsMMP14 expression was elevated in SMCs within fibroatheroma compared with the pathological intima thickening in coronary aortas from patients with ASCVD. Conditional knockout of SMC MMP14 in adult mice did not change plasma cholesterol levels or basic cardiac and vascular function. However, atherosclerosis development was reduced, and the regression of existing plaques was enhanced in Ldlr
conclusionSMC MMP14 promotes atherosclerosis in adult mice, likely through reducing PDGF signalling and inhibiting SMC migration and proliferation.
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