ArticleScientific reports2025
Systemic downregulation of EV-associated MiRNAs following remote ischemic preconditioning.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07487220 (Non-invasive Remote Ischemic PreConditioning in Free Flaps for Breast Reconstruction), which is not on this map. Cited by 1 paper.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Non-invasive Remote Ischemic PreConditioning in Free Flaps for Breast Reconstruction
Who cites it
1 citing paper in PubMed.
- Uncovering the dynamics of extracellular vesicle microRNA trafficking in multiple sclerosis: delivery, diversion and retention.Extracellular vesicles and circulating nucleic acids · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Remote ischemic preconditioning (RIPC) is a non-invasive strategy to protect tissues from ischemia-reperfusion injury (IRI), yet its systemic molecular mediators remain incompletely understood. Extracellular vesicles (EVs), particularly their microRNA (miRNA) cargo, have emerged as potential conveyors of RIPC-induced protection. In this translational study, we performed paired EV-miRNA profiling in five human subjects undergoing free flap surgery, with plasma collected before and 30 min after a standardized RIPC protocol. EVs were isolated, RNA was extracted and profiled using a 384-plex qPCR array. Differential expression was assessed using paired statistics and false discovery correction. Functional impact was inferred via validated target mapping, gene set enrichment analysis (GSEA), and miRNA-gene-pathway network modeling. RIPC induced a rapid, systemic shift in the circulating EV-miRNA profile. Principal component analysis revealed consistent directional changes post-RIPC. Four miRNAs, hsa-miR-505-3p (log2FC = -3.30, p = 0.025), hsa-miR-374a-5p (log2FC = -4.52, p = 0.028), hsa-miR-200a-3p (log2FC = -7.27, p = 0.044), and hsa-miR-181b-5p (log2FC = -3.94, p = 0.045), were significantly downregulated across the cohort. No miRNAs were consistently upregulated. GSEA of validated targets showed positive enrichment of stress-responsive and pro-survival pathways, including TNF-alpha signaling, TGF-beta, Notch, hypoxia, angiogenesis, and apoptosis. Network analysis identified miR-181b-5p and miR-374a-5p as central regulators affecting multiple interconnected pathways. These results suggest that RIPC elicits systemic protection not by introducing new molecular signals but by selectively removing suppressive EV-bound miRNAs. This may reflect a subtractive regulatory mechanism and enable rapid derepression of protective gene programs, offering a plausible explanation for the early benefits of RIPC. These findings should be validated in larger, multi-timepoint cohorts.
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Registered trials
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