ArticleFrontiers in oncology2025
Functions and mechanisms of UC-MSC-derived exosomal miR-486-5p in pulmonary fibrosis.
Article in Frontiers in oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed, 1 synthesis or guideline pooled it.
- MicroRNA regulation in pulmonary fibrosis: a bibliometric analysis of global research trends, collaborative networks, and emerging frontiers.Frontiers in medicine · 2026Pooled it
- Mesenchymal stem/stromal cell-based therapies for autism spectrum disorder: emerging evidence and clinical prospects.Journal of translational medicine · 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
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Currently, nintedanib and pirfenidone are the two primary pharmacological agents used to treat pulmonary fibrosis (PF). However, neither of these medications effectively halts the progression of PF or preserves lung function. As a result, lung transplantation remains the sole viable treatment option for patients in the advanced stages of the disease. Therefore, it is imperative to identify new therapeutic agents that can more effectively address this condition. Methods: Exosomes were harvested from the supernatants of human umbilical cord-derived mesenchymal stem cells (UC-MSCs) transfected with either control or miR-486-5p-overexpressing lentivirus via ultracentrifugation and subsequently resuspended in minimum essential medium (MEM). The immunophenotypes were analyzed by Western blotting, and their concentration was determined using the Nanoparticle Tracking Analysis device, NanoSight NS300. The influence of exosomal microRNA-486-5p (miR-486-5p) derived from UC-MSCs on apoptosis in MRC-5 cells was assessed using flow cytometry, and cell proliferation was evaluated through the CCK-8 assay. The expression levels of miR-486-5p, fibroblast growth factor 9 (FGF9), and extracellular matrix (ECM)-related genes were quantified through quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Results: MiR-486-5p inhibits TGF-β 1-induced pulmonary fibroblast differentiation by targeting FGF9. Exogenous exosomes facilitate the transfer of miR-486-5p to MRC-5 cells. The presence of exosomal miR-486-5p reduces the mRNA expression of FGF9, fibronectin (Fn), alpha-smooth muscle actin (α-SMA), vimentin, COL1A1, and COL3A1, and decreases FGF9 and vimentin protein levels. Compared to control exosomes, UC-MSC-derived exosomal miR-486-5p slightly promotes apoptosis in MRC-5 cells ( Conclusion: Exosomal miR-486-5p derived from UC-MSCs shows potential therapeutic efficacy in regulating fibroblast differentiation by targeting FGF9, thereby mitigating the progression of PF.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.