ArticleAmerican journal of respiratory cell and molecular biology2016
MicroRNA-27a-3p Is a Negative Regulator of Lung Fibrosis by Targeting Myofibroblast Differentiation.
Article in American journal of respiratory cell and molecular biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 1 of them a synthesis that pooled it.
What it found
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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
55 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Systematic review of overlapping microRNA patterns in COVID-19 and idiopathic pulmonary fibrosis.Respiratory research · 2023Pooled it
- Circulating microRNA profiles predict the severity of COVID-19 in hospitalized patients.Translational research : the journal of laboratory and clinical medicine · 2021Trial
- Recent advances on anti-scarring properties of amniotic membrane: emerging strategies and clinical potentials in regenerative medicine.Stem cell research & therapy · 2026Review
- Exosomes as Disease-Informed Nanoplatforms for Pulmonary Fibrosis: From Pathogenic Signaling to Precision Diagnosis and Therapy.Pharmaceutics · 2026Review
- Isoform-Specific Control of Adipose Thermogenesis by the miR-27 Family Reveals Antagonism within a Polycistronic miRNA Cluster.bioRxiv : the preprint server for biology · 2026Article
- BMAL1 regulates tubular epithelial-derived exosomal miR-27a-3p to inhibit macrophage-myofibroblast transition and alleviate ischemia/reperfusion-induced renal fibrosis.Theranostics · 2026Article
- MicroRNAs in Systemic Sclerosis: Involvement in Disease Pathogenesis and Potential Use as Diagnostic Biomarkers and Therapeutic Targets.Biomedicines · 2025Review
- Extracellular vesicles derived from bone marrow mesenchymal stem cells ameliorate liver fibrosis via micro-7045-5p.Molecular and cellular biochemistry · 2025Article
- Review
- Review
- Mechanisms and Therapeutic Potential of Myofibroblast Transformation in Pulmonary Fibrosis.Journal of respiratory biology and translational medicine · 2025Article
- miR-27a-3p regulates intestinal cell proliferation and differentiation through Wnt/β-catenin signalling.Cell proliferation · 2025Article
- Therapeutic applications of stem cell-derived exosomes in radiation-induced lung injury.Cancer cell international · 2024Review
- Dihydroartemisinin (DHA) inhibits myofibroblast differentiation through inducing ferroptosis mediated by ferritinophagy.Heliyon · 2024Article
- Emerging roles of non-coding RNAs in fibroblast to myofibroblast transition and fibrotic diseases.Frontiers in pharmacology · 2024Review
- Revisiting the role of MicroRNAs in the pathogenesis of idiopathic pulmonary fibrosis.Frontiers in cell and developmental biology · 2024Review
- Delivery of anti-microRNA-21 by lung-targeted liposomes for pulmonary fibrosis treatment.Molecular therapy. Nucleic acids · 2023Article
- Extracellular vesicles: A promising therapy against SARS-CoV-2 infection.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Article
- miRNA Expression in Fibroblastic Foci within Idiopathic Pulmonary Fibrosis Lungs Reveals Novel Disease-Relevant Pathways.The American journal of pathology · 2023Article
- Noncoding RNAs: Master Regulator of Fibroblast to Myofibroblast Transition in Fibrosis.International journal of molecular sciences · 2023Review
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Although microRNAs (miRs) have been well recognized to play an important role in the pathogenesis of organ fibrosis, there is a lack of evidence as to whether miRs directly regulate the differentiation of myofibroblasts, the putative effector cells during pathological fibrogenesis. In this study, we found that levels of miR-27a-3p were up-regulated in transforming growth factor-β1-treated human lung fibroblasts in a Smad2/3-dependent manner and in fibroblasts isolated from lungs of mice with experimental pulmonary fibrosis. However, both basal and transforming growth factor-β1-induced expression of miR-27a-3p were reduced in lung fibroblasts from patients with idiopathic pulmonary fibrosis compared with that from normal control subjects. Overexpression of miR-27a-3p inhibited, whereas knockdown of miR-27a-3p enhanced, the differentiation of lung fibroblasts into myofibroblasts. We found that miR-27a-3p directly targeted the phenotypic marker of myofibroblasts, α-smooth muscle actin, and two key Smad transcription factors, Smad2 and Smad4. More importantly, we found that therapeutic expression of miR-27a-3p in mouse lungs through lentiviral delivery diminished bleomycin-induced lung fibrosis. In conclusion, our data suggest that miR-27a-3p functions via a negative-feedback mechanism in inhibiting lung fibrosis. This study also indicates that targeting miR-27a-3p is a novel therapeutic approach to treat fibrotic organ disorders, including lung fibrosis.
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