ArticlePloS one2025
FoxO3a regulated by miR-150-5p promotes the pyroptosis of macrophages in atherosclerosis.
Article in PloS one, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- NLRP3-mediated pyroptosis in cardiovascular disease: from molecular mechanisms to therapeutic targets.Frontiers in pharmacology · 2026Review
- Advances in Exosome Research in Renal Cell Carcinoma: Mechanisms, Biomarkers, and Therapeutic Applications.International journal of nanomedicine · 2026Review
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThis study uses tissue exosome analysis to explore the role of miR-150-5p and its downstream genes in atherosclerosis (AS), an area where the functional mechanisms and pathophysiological significance of exosomal miR-150-5p remain poorly understood.
methodsExosomes from AS mouse vascular tissue were analyzed to identify miR-150-5p target genes. Dual luciferase assays validated miRNA-target interactions, while RT-qPCR and Western blot assessed FoxO3a expression. RNA interference studies determined FoxO3a's role in pyroptosis. In vivo efficacy of the miR-150-5p inhibitor was evaluated using HE, Masson staining, and immunofluorescence.
resultsIn AS tissue exosomes, miR-150-5p levels increased whereas FoxO3a levels decreased. miR-150-5p regulated FoxO3a, enhancing macrophage pyroptosis. The miR-150-5p inhibitor reduced ox-LDL-induced RAW264.7 injury and pyroptosis by improving cell viability, decreasing LDH levels, and downregulating pyroptosis related proteins (Caspase-1, NLRP3, GSDMD-N). FoxO3a knockdown weakened the inhibitor's effects on NLRP3/GSDMD-mediated pyroptosis. In Apoe-/- mice, the inhibitor upregulated FoxO3a/ARC and suppressed pyroptosis signaling.
conclusionThis study advances understanding of miR-150-5p-mediated pyroptosis and highlights the potential of miR-150-5p inhibitors in combating AS.
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