ArticleCell death & disease2019
Transforming growth factor (TGF)-β1-induced miR-133a inhibits myofibroblast differentiation and pulmonary fibrosis.
Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 103 papers, 1 of them a synthesis 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
103 citing papers in PubMed, 1 synthesis or guideline pooled it, 158 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
- Polyplex of peptide-mannan and RNA for intranasal delivery of TGF-β siRNA in treatment of pulmonary fibrosis.Bioactive materials · 2026Article
- Atorvastatin Attenuates Human Cardiac Fibroblast Activation, with Associated Changes in GATA4/MEF2C and Selected Fibrosis-Related microRNAs.International journal of molecular sciences · 2026Article
- The antifibrotic effects of a click chemistry-based albumin nanocomplex in an idiopathic pulmonary fibrosis model.Journal of nanobiotechnology · 2026Article
- Emerging roles of microRNAs and other non-coding transcriptome in muscular dystrophies.Inflammation and regeneration · 2026Review
- Targeting the DNA damage repair protein RAD51 alters fibroblast metabolism and enhances apoptosis in pulmonary fibrosis.bioRxiv : the preprint server for biology · 2026Article
- Therapeutic Potential of Lentiviral miR-200a Mimics in Regulating Fibrinolysis and EMT Markers During Pulmonary Fibrosis.FASEB bioAdvances · 2026Article
- Article
- Polystyrene-associated pulmonary fibrosis: a summary based on the available evidence and prospects.Frontiers in immunology · 2026Review
- A deep generative model for deciphering cellular dynamics and in silico drug discovery in complex diseases.Nature biomedical engineering · 2025Article
- Circulating miR-145-5p and miR-133a-3p in pediatric sickle cell disease: biomarker potential for vaso-occlusive crises and disease activity.Annals of hematology · 2025Article
- FAK-dependent activation of src family kinase member BLK contributed to endometrial fibrosis via endoplasmic reticulum stress.Cell & bioscience · 2025Article
- The role of CARMA3 in regulating fibrosis to prevent hypertrophic cardiomyopathy.Cell death discovery · 2025Article
- 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
- Article
- Deciphering the interplay: circulating cell-free DNA, signaling pathways, and disease progression in idiopathic pulmonary fibrosis.3 Biotech · 2025Review
- The role of MicroRNAs in mesenchymal stem cell differentiation into vascular smooth muscle cells.Cell division · 2025Review
- Mechanisms and Therapeutic Potential of Myofibroblast Transformation in Pulmonary Fibrosis.Journal of respiratory biology and translational medicine · 2025Article
- MicroRNAs as promising drug delivery target to ameliorate chronic obstructive pulmonary disease using nano-carriers: a comprehensive review.Molecular and cellular biochemistry · 2025Review
- Proteomic Approach to Study the Effect ofJournal of fungi (Basel, Switzerland) · 2025Article
43 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
10 authors at 6 institutions in 2 countries.
Funding
Abstract
Transforming growth factor (TGF)-β1, a main profibrogenic cytokine in the progression of idiopathic pulmonary fibrosis (IPF), induces differentiation of pulmonary fibroblasts to myofibroblasts that produce high levels of collagen, leading to concomitantly loss of lung elasticity and function. Recent studies implicate the importance of microRNAs (miRNAs) in IPF but their regulation and individual pathological roles remain largely unknown. We used both RNA sequencing and quantitative RT-PCR strategies to systematically study TGF-β1-induced alternations of miRNAs in human lung fibroblasts (HFL). Our data show that miR-133a was significantly upregulated by TGF-β1 in a time- and concentration-dependent manner. Surprisingly, miR-133a inhibits TGF-β1-induced myofibroblast differentiation whereas miR-133a inhibitor enhances TGF-β1-induced myofibroblast differentiation. Interestingly, quantitative proteomics analysis indicates that miR-133a attenuates myofibroblast differentiation via targeting multiple components of TGF-β1 profibrogenic pathways. Western blot analysis confirmed that miR-133a down-regulates TGF-β1-induced expression of classic myofibroblast differentiation markers such as ɑ-smooth muscle actin (ɑ-SMA), connective tissue growth factor (CTGF) and collagens. miRNA Target Searcher analysis and luciferase reporter assays indicate that TGF-β receptor 1, CTGF and collagen type 1-alpha1 (Col1a1) are direct targets of miR-133a. More importantly, miR-133a gene transferred into lung tissues ameliorated bleomycin-induced pulmonary fibrosis in mice. Together, our study identified TGF-β1-induced miR-133a as an anti-fibrotic factor. It functions as a feed-back negative regulator of TGF-β1 profibrogenic pathways. Thus, manipulations of miR-133a expression may provide a new therapeutic strategy to halt and perhaps even partially reverse the progression of IPF.
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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 OpenQuestion graph.