ArticleThe Journal of international medical research2023
MicroRNA-22-3p alleviates atherosclerosis by mediating macrophage M2 polarization as well as inhibiting NLRP3 activation.
Article in The Journal of international medical research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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.
The trial behind it
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Who cites it
5 citing papers in PubMed, 6 citations in OpenAlex.
- MicroRNA Profiling of the Pathophysiological Mechanisms Underlying Carotid Atherosclerosis Progression.Biomolecules · 2026Review
- Macrophage microRNAs integrating lipid metabolism and inflammation: Implications for atherosclerosis.Metabolism open · 2026Review
- Exosomes and microRNA - a new form of remote and bidirectional neuroimmunomodulation?Neuroimmunomodulation · 2025Review
- miR-214-3p Promotes ox-LDL-Induced Macrophages Ferroptosis and Inflammation via GPX4.Journal of inflammation research · 2025Article
- Role of ncRNAs in the Pathogenesis of Sjögren's Syndrome.Biomedicines · 2024Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveMicroRNA (miR)-22-3p is expressed in atherosclerosis (AS), but its function and regulatory mechanisms remain unclear. Therefore, the effects of miR-22-3p in AS were assessed in this study.
methodsMiR-22-3p expression was assessed in AS, and miR-22-3p target genes were predicted using sequencing transcriptomics. The effect of miR-22-3p agomir on atherosclerotic lesions in an AS mouse model were determined by Oil red O, Masson's, and sirius red staining, and by anti-smooth muscle actin and macrophage antigen-3 immunostaining. Gene expression in AS was evaluated by western blot and immunofluorescence.
resultsMiR-22-3p was expressed in AS and control samples (32.5% and 33.9% levels, respectively, relative to total miRNA among six highly expressed miRNAs). In the mouse model of AS, miR-22-3p agomir significantly reduced lipid deposition, proliferation of aortic collagen fibres, and macrophage content. Additionally, inducible nitric oxide synthase, interleukin-6, and tumour necrosis factor-α levels were significantly reduced, and levels of arginase 1 and CD206 were significantly enhanced. MiR-22-3p was found to target janus kinase 1(
conclusionsMiR-22-3p appears to reduce the inflammatory response in AS, which might be achieved by inducing the M2 macrophage phenotype and suppressing NLRP3 activation via JAK1.
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Registered trials
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