Mir147 Limits the Contribution of Non-Foamy Macrophages to Atherosclerosis
Authors' conclusion
miR-147-3p reduces atherosclerosis by suppressing the harmful effects of NFMs on endothelial cells and by enhancing their clearance of apoptotic DNA through targeting galectin-3.
Study context
- Population
- Apoe-/- mice with myeloid cell-specific Mir147 knockout; mouse and human atherosclerosis
- Comparison
- Myeloid Mir147 knockout vs Mir147-intact Apoe-/- mice
Methodological detailsmyeloid cell-specific knockout, Apoe-/- mice, live-plaque 4D confocal imaging
- Myeloid cell-specific knockout
- Apoe-/- mice
- Live-plaque 4D confocal imaging
Main finding
As reported in the abstract
- Non-foamy macrophages (NFMs) mainly in plaque core, with higher miR-147-3p levels than foamy macrophages (FMs) in mouse and human atherosclerosis
- Myeloid Mir147 knockout increases atherosclerosis, with enhanced cholesterol crystal (CC) formation and apoptotic DNA accumulation in necrotic cores
- Mir147 removal reduces mitochondrial activity and raises caspase-3 activity in NFMs, not FMs; lowers spare respiratory capacity of plaque macrophages
- Mir147 deletion impairs NFM uptake of apoptotic DNA, increases extracellular apoptotic DNA, promotes CC formation
- Mir147 deficiency in NFMs induces endothelial caspase-3 activation, facilitating transendothelial extension of FM projections
- Lgals3 (galectin-3) transcript reduced in tAgo2 immunoprecipitate after knockout; miR-147-3p binding site in Lgals3 3'-UTR functionally confirmed
- Galectin-3 inhibitor GB1107 reversed the Mir147 knockout effect in macrophages
Original publication
Mir147 Limits the Contribution of Non-Foamy Macrophages to Atherosclerosis. Circulation. Published 7 April 2026. doi:10.
Summarised from the published abstract; every number is checked against it