ArticleJCI insight2016
miR-323a-3p regulates lung fibrosis by targeting multiple profibrotic pathways.
Article in JCI insight, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 2 of them syntheses that pooled it.
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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.
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Who cites it
28 citing papers in PubMed, 2 syntheses or guidelines pooled it, 48 citations in OpenAlex.
- Interception of Regulatory RNAs on TGF-β Signaling in the Pathogenesis of Idiopathic Pulmonary Fibrosis: A Systematic Review.Current allergy and asthma reports · 2026Pooled it
- Effects of AntagomiRs on Different Lung Diseases in Human, Cellular, and Animal Models.International journal of molecular sciences · 2019Pooled it
- Circulating miRNA-Protein Signatures Predict Outcomes in Pediatric Dilated Cardiomyopathy.bioRxiv : the preprint server for biology · 2026Article
- LncRNA SYISL promotes fibroblast myofibroblast transition via miR-23a-mediated TRIOBP regulation.Cellular and molecular life sciences : CMLS · 2025Article
- Review
- Circulating cell-free and extracellular vesicles-derived microRNA as prognostic biomarkers in patients with early-stage NSCLC: results from RESTING study.Journal of experimental & clinical cancer research : CR · 2024Observational
- Arrestin beta 1 Regulates Alveolar Progenitor Renewal and Lung Fibrosis.Journal of respiratory biology and translational medicine · 2024Article
- Revisiting the role of MicroRNAs in the pathogenesis of idiopathic pulmonary fibrosis.Frontiers in cell and developmental biology · 2024Review
- Advanced models for respiratory disease and drug studies.Medicinal research reviews · 2023Review
- Role of MicroRNAs in Signaling Pathways Associated with the Pathogenesis of Idiopathic Pulmonary Fibrosis: A Focus on Epithelial-Mesenchymal Transition.International journal of molecular sciences · 2022Review
- Targeting Histone Deacetylases in Idiopathic Pulmonary Fibrosis: A Future Therapeutic Option.Cells · 2022Review
- Inhibition of nuclear factor κB in the lungs protect bleomycin-induced lung fibrosis in mice.Molecular biology reports · 2022Article
- Review
- MicroRNA-323a-3p Negatively Regulates NEK6 in Colon Adenocarcinoma Cells.Journal of oncology · 2022Article
- miRNAs, from Evolutionary Junk to Possible Prognostic Markers and Therapeutic Targets in COVID-19.Viruses · 2021Review
- Deciphering the role of microRNAs in mustard gas-induced toxicity.Annals of the New York Academy of Sciences · 2021Review
- Role of Non-Coding RNAs in Post-Transcriptional Regulation of Lung Diseases.Frontiers in genetics · 2021Review
- The function of non-coding RNAs in idiopathic pulmonary fibrosis.Open medicine (Warsaw, Poland) · 2021Review
- Modulation of miRNAs by vitamin C in H2O2‑exposed human umbilical vein endothelial cells.International journal of molecular medicine · 2020Article
- Ischemia/reperfusion injured intestinal epithelial cells cause cortical neuron death by releasing exosomal microRNAs associated with apoptosis, necroptosis, and pyroptosis.Scientific reports · 2020Article
Corrections and comments
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Authors and funding
18 authors at 4 institutions in 2 countries.
Funding
Abstract
Maladaptive epithelial repair from chronic injury is a common feature in fibrotic diseases, which in turn activates a pathogenic fibroblast response that produces excessive matrix deposition. Dysregulated microRNAs (miRs) can regulate expression of multiple genes and fundamentally alter cellular phenotypes during fibrosis. Although several miRs have been shown to be associated with lung fibrosis, the mechanisms by which miRs modulate epithelial behavior in lung fibrosis are lacking. Here, we identified miR-323a-3p to be downregulated in the epithelium of lungs with bronchiolitis obliterans syndrome (BOS) after lung transplantation, idiopathic pulmonary fibrosis (IPF), and murine bleomycin-induced fibrosis. Antagomirs for miR-323a-3p augment, and mimics suppress, murine lung fibrosis after bleomycin injury, indicating that this miR may govern profibrotic signals. We demonstrate that miR-323a-3p attenuates TGF-α and TGF-β signaling by directly targeting key adaptors in these important fibrogenic pathways. Moreover, miR-323a-3p lowers caspase-3 expression, thereby limiting programmed cell death from inducers of apoptosis and ER stress. Finally, we find that epithelial expression of miR-323a-3p modulates inhibitory crosstalk with fibroblasts. These studies demonstrate that miR-323a-3p has a central role in lung fibrosis that spans across murine and human disease, and downregulated expression by the lung epithelium releases inhibition of various profibrotic pathways to promote fibroproliferation.
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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.