ReviewFrontiers in cell and developmental biology2024
Revisiting the role of MicroRNAs in the pathogenesis of idiopathic pulmonary fibrosis.
Review in Frontiers in cell and developmental biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed.
- Article
- Why males scar more: hormonal and chromosomal clues to idiopathic pulmonary fibrosis.Biology of sex differences · 2026Article
- Aging alters synergistic microRNA networks in exosomes to stimulate repair in lung injury and skin wound healing.Molecular therapy. Nucleic acids · 2026Article
- Exosomes as Disease-Informed Nanoplatforms for Pulmonary Fibrosis: From Pathogenic Signaling to Precision Diagnosis and Therapy.Pharmaceutics · 2026Review
- Integrative Machine Learning and Structural Modeling Identify Multitarget Therapeutic Candidates for Idiopathic Pulmonary Fibrosis.ACS omega · 2026Article
- Therapeutic Potential of Lentiviral miR-200a Mimics in Regulating Fibrinolysis and EMT Markers During Pulmonary Fibrosis.FASEB bioAdvances · 2026Article
- Exploring the role of epigenetics in the processes related to the development of endometrosis in the mare.The Journal of reproduction and development · 2026Review
- The emerging roles of microRNAs in pneumoconiosis: pathogenic mechanisms and clinical implications.Frontiers in cell and developmental biology · 2026Review
- miR-146b disrupts the epidermal growth factor receptor/transforming growth factor β receptor profibrotic feedforward loop to inhibit lung fibroblast proliferation and differentiation.The Journal of pharmacology and experimental therapeutics · 2025Article
- Review
- Air pollution and alveolar health.European respiratory review : an official journal of the European Respiratory Society · 2025Review
- [Pathophysiology of fibrosis: inflammatory vs. non-inflammatory].Innere Medizin (Heidelberg, Germany) · 2025Review
- Advances in Therapeutics for Chronic Lung Diseases: From Standard Therapies to Emerging Breakthroughs.Journal of clinical medicine · 2025Review
- Pathological Mechanisms of Radiation-Induced Lung Injury and Novel Nano-Drug Delivery Therapeutic Strategies.International journal of nanomedicine · 2025Review
- Recent progress in exosomal non-coding RNAs research related to idiopathic pulmonary fibrosis.Frontiers in genetics · 2025Review
- Identification of glycolysis-related gene signatures for prognosis and therapeutic targeting in idiopathic pulmonary fibrosis.Frontiers in pharmacology · 2025Article
- Circulating MicroRNAs in Idiopathic Pulmonary Fibrosis: A Narrative Review.Current issues in molecular biology · 2024Review
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Idiopathic pulmonary fibrosis (IPF) is a prevalent chronic pulmonary fibrosis disease characterized by alveolar epithelial cell damage, fibroblast proliferation and activation, excessive extracellular matrix deposition, and abnormal epithelial-mesenchymal transition (EMT), resulting in tissue remodeling and irreversible structural distortion. The mortality rate of IPF is very high, with a median survival time of 2-3 years after diagnosis. The exact cause of IPF remains unknown, but increasing evidence supports the central role of epigenetic changes, particularly microRNA (miRNA), in IPF. Approximately 10% of miRNAs in IPF lung tissue exhibit differential expression compared to normal lung tissue. Diverse miRNA phenotypes exert either a pro-fibrotic or anti-fibrotic influence on the progression of IPF. In the context of IPF, epigenetic factors such as DNA methylation and long non-coding RNAs (lncRNAs) regulate differentially expressed miRNAs, which in turn modulate various signaling pathways implicated in this process, including transforming growth factor-β1 (TGF-β1)/Smad, mitogen-activated protein kinase (MAPK), and phosphatidylinositol-3-kinase/protein kinase B (PI3K/AKT) pathways. Therefore, this review presents the epidemiology of IPF, discusses the multifaceted regulatory roles of miRNAs in IPF, and explores the impact of miRNAs on IPF through various pathways, particularly the TGF-β1/Smad pathway and its constituent structures. Consequently, we investigate the potential for targeting miRNAs as a treatment for IPF, thereby contributing to advancements in IPF research.
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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 Socratic graph.