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• W2344659999 abstract "Abnormal remodeling of atherosclerotic plaques can lead to rupture, acute myocardial infarction, and death. Enhancement of plaque extracellular matrix (ECM) may improve plaque morphology and stabilize lesions. Here, we demonstrate that chronic administration of LNA-miR-29 into an atherosclerotic mouse model improves indices of plaque morphology. This occurs due to upregulation of miR-29 target genes of the ECM (col1A and col3A) resulting in reduced lesion size, enhanced fibrous cap thickness, and reduced necrotic zones. Sustained LNA-miR-29 treatment did not affect circulating lipids, blood chemistry, or ECM of solid organs including liver, lung, kidney, spleen, or heart. Collectively, these data support the idea that antagonizing miR-29 may promote beneficial plaque remodeling as an independent approach to stabilize vulnerable atherosclerotic lesions." @default.
• W2344659999 created "2016-06-24" @default.
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• W2344659999 date "2016-05-02" @default.
• W2344659999 modified "2023-10-17" @default.
• W2344659999 title "Chronic miR‐29 antagonism promotes favorable plaque remodeling in atherosclerotic mice" @default.
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• W2344659999 doi "https://doi.org/10.15252/emmm.201506031" @default.
• W2344659999 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4888854" @default.
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