ArticleMolecular therapy : the journal of the American Society of Gene Therapy2014
The antifibrotic effects and mechanisms of microRNA-26a action in idiopathic pulmonary fibrosis.
Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 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
82 citing papers in PubMed, 1 synthesis or guideline pooled it, 128 citations in OpenAlex.
- A systematic review of overlapping microRNA patterns in systemic sclerosis and idiopathic pulmonary fibrosis.European respiratory review : an official journal of the European Respiratory Society · 2017Pooled it
- Expression Analysis of Selected miRNAs in COVID-19 Patients.Microorganisms · 2026Article
- The Role of Epigenetics in Corneal Fibrosis.Epigenomes · 2026Review
- Multi-omics approaches in idiopathic pulmonary fibrosis: from molecular mechanisms to therapeutic targets and precision medicine.Frontiers in pharmacology · 2026Review
- Systemic miR-26a deficiency attenuates pulmonary fibrosis via PTEN upregulation and downstream TIMP-1 suppression.Molecular therapy. Nucleic acids · 2025Article
- Integrative Metabolomic, Network Pharmacology, and Experimental Evidence forPharmaceuticals (Basel, Switzerland) · 2025Article
- Association of fibrotic-related extracellular vesicle microRNAs with lung involvement in systemic sclerosis.The European respiratory journal · 2025Article
- An Overview of the Role of Genetic factors in Idiopathic Pulmonary Fibrosis: Insights from Epidemiology to Prognosis.International journal of medical sciences · 2025Review
- Memantine/Rosuvastatin Therapy Abrogates Cognitive and Hippocampal Injury in an Experimental Model of Alzheimer's Disease in Rats: Role of TGF-β1/Smad Signaling Pathway and Amyloid-β Clearance.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2024Article
- MicroRNA-26a in respiratory diseases: mechanisms and therapeutic potential.Molecular biology reports · 2024Review
- Drugs targeting CTGF in the treatment of pulmonary fibrosis.Journal of cellular and molecular medicine · 2024Review
- Epigenetic Regulation of EMP/EMT-Dependent Fibrosis.International journal of molecular sciences · 2024Review
- Regulation of idiopathic pulmonary fibrosis: a cross-talk between TGF-Frontiers in medicine · 2024Review
- Revisiting the role of MicroRNAs in the pathogenesis of idiopathic pulmonary fibrosis.Frontiers in cell and developmental biology · 2024Review
- Mesenchymal stem cell-derived exosomal miR-26a induces ferroptosis, suppresses hepatic stellate cell activation, and ameliorates liver fibrosis by modulating SLC7A11.Open medicine (Warsaw, Poland) · 2024Article
- Advances in the Study of Non-Coding RNA in the Signaling Pathway of Pulmonary Fibrosis.International journal of general medicine · 2024Review
- Delivery of anti-microRNA-21 by lung-targeted liposomes for pulmonary fibrosis treatment.Molecular therapy. Nucleic acids · 2023Article
- miRNA Expression in Fibroblastic Foci within Idiopathic Pulmonary Fibrosis Lungs Reveals Novel Disease-Relevant Pathways.The American journal of pathology · 2023Article
- Exosome‑encapsulated miR‑26a attenuates aldosterone‑induced tubulointerstitial fibrosis by inhibiting the CTGF/SMAD3 signaling pathway.International journal of molecular medicine · 2023Article
- Boosting therapeutic efficacy of mesenchymal stem cells in pulmonary fibrosis: The role of genetic modification and preconditioning strategies.Iranian journal of basic medical sciences · 2023Review
22 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive, and high-lethality fibrotic lung disease characterized by excessive fibroblast proliferation, extracellular matrix accumulation, and, ultimately, loss of lung function. Although dysregulation of some microRNAs (miRs) has been shown to play important roles in the pathophysiological processes of IPF, the role of miRs in fibrotic lung diseases is not well understood. In this study, we found downregulation of miR-26a in the lungs of mice with experimental pulmonary fibrosis and in IPF, which resulted in posttranscriptional derepression of connective tissue growth factor (CTGF), and induced collagen production. More importantly, inhibition of miR-26a in the lungs caused pulmonary fibrosis in vivo, whereas overexpression of miR-26a repressed transforming growth factor (TGF)-β1-induced fibrogenesis in MRC-5 cells and attenuated experimental pulmonary fibrosis in mice. Our study showed that miR-26a was downregulated by TGF-β1-mediated phosphorylation of Smad3. Moreover, miR-26a inhibited the nuclear translocation of p-Smad3 through directly targeting Smad4, which determines the nuclear translocation of p-Smad2/Smad3. Taken together, our experiments demonstrated the antifibrotic effects of miR-26a in fibrotic lung diseases and suggested a new strategy for the prevention and treatment of IPF using miR-26a. The current study also uncovered a novel positive feedback loop between miR-26a and p-Smad3, which is involved in pulmonary fibrosis.
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.