ArticleCellular and molecular life sciences : CMLS2026
Endothelial EV-derived miR-122b-3p suppresses autophagy via FOXP1/FUT8- dependent core fucosylation in uremic coronary artery calcification.
Article in Cellular and molecular life sciences : CMLS, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Cardiovascular disease is the leading cause of mortality in patients with hemodialysis. Coronary artery calcification represents a major pathological substrate and an independent risk factor for adverse cardiovascular outcomes. Although endothelial-smooth muscle cell crosstalk is critical in vascular calcification and extracellular vesicles (EVs) are key intercellular mediators, their role in coronary artery calcification remains unexplored. Additionally, the mechanisms linking α-1,6-fucosyltransferase (FUT8) upregulation in calcified vascular smooth muscle cells to endothelial EV signaling are unknown. High phosphorus and high calcium conditions were applied to coronary artery endothelial cells to induce EV secretion. The EVs were isolated and characterized, and their uptake by coronary artery smooth muscle cells was examined. Molecular analyses assessed the effects of EV-derived miR-122b-3p on FOXP1 repression, FUT8 expression, integrin αV (ITGAV) core fucosylation, and autophagy suppression. Endothelial EVs were highly enriched with miR-122b-3p under calcifying conditions and were internalized by smooth muscle cells, leading to FOXP1 repression, FUT8 upregulation, enhanced ITGAV core fucosylation, autophagy suppression, and accelerated coronary artery calcification. In uremic rats, EVs overexpressing miR-122b-3p aggravated coronary artery calcification by modulating the FOXP1/ FUT8/ITGAV signaling pathway. Preliminary analysis of serum EVs from healthy controls and patients with CKD/uremia further showed increased serum EV miR-122b-3p levels and associations with renal dysfunction and mineral metabolism-related parameters, supporting the potential clinical relevance of this EV-miRNA axis. This study identifies a novel extracellular vesicle-dependent intercellular communication mechanism linking FUT8-mediated core fucosylation to autophagy dysfunction in coronary artery calcification.
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