ArticleAmerican journal of respiratory cell and molecular biology2011
miR-29 is a major regulator of genes associated with pulmonary fibrosis.
Article in American journal of respiratory cell and molecular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 306 papers.
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Who cites it
306 citing papers in PubMed, 488 citations in OpenAlex.
- circHIPK3 promotes pro-fibrotic epithelial reprogramming via the miR-29a-3p/SPARC axis with associated enhancement of TGF-β/SMAD signaling.Non-coding RNA research · 2026Article
- miR-29b as an Anti-Fibrotic Therapeutic: Mechanisms, Disease Biology and Translational Opportunities.Cells · 2026Review
- Transitional cell states at the crossroads of development, disease, and repair-regeneration.Physiological reviews · 2026Review
- Why males scar more: hormonal and chromosomal clues to idiopathic pulmonary fibrosis.Biology of sex differences · 2026Article
- The Genetic Landscape of Fibrotic Interstitial Lung Diseases: Clinical Implications and Diagnostic Challenges in Familial Pulmonary Fibrosis.Journal of clinical medicine · 2026Review
- Unraveling mortality risk in pediatric acute respiratory distress syndrome: key biomarkers and pathophysiological insights.Pediatric research · 2026Review
- Heart-Lung Interactions in Pulmonary Hypertension due to Heart Failure With Preserved Ejection Fraction.Comprehensive physiology · 2026Review
- Review
- Human Corneal Stromal Stem Cell Treatment Reduces Established Opacities in Chronic Corneal Scarring.Cells · 2026Article
- The extracellular matrix: structure, composition, biological functions, diseases, and therapeutic targets.Molecular biomedicine · 2026Review
- Study of circulating MiRNA expression in myopic patients.International ophthalmology · 2026Article
- Myofibroblast lineage mapping and inhibiting subretinal fibrosis by targeting SMAD3 and MRTF pathways via microRNA-24 functional study.bioRxiv : the preprint server for biology · 2026Article
- The Role of Non-Coding RNAs in the Pathogenesis and Progression of Diabetic Kidney Disease.International journal of molecular sciences · 2026Review
- Circulating MicroRNAs as Biomarkers for Cardiovascular Events: Bioinformatics and Machine Learning Approaches.Methods in molecular biology (Clifton, N.J.) · 2026Review
- Improved wound healing by dual inhibition of miR-146a-5p and miR-29a-3p supports a network action of dysregulated miRNAs in diabetic skin.Diabetologia · 2026Article
- Identification of candidate selenium-associated transcriptomic biomarkers in chronic obstructive pulmonary disease: an integrated bioinformatics and expression validation study.Frontiers in medicine · 2026Article
- Curcumin in Fibrosis Treatment: A Review.Drug design, development and therapy · 2026Review
- Intestinal subepithelial myofibroblasts in inflammatory bowel disease: fibroblast heterogeneity, fibrosis, and therapeutic targeting.Frontiers in medicine · 2026Review
- Idiopathic Pulmonary Fibrosis: Cellular Heterogeneity, Mechanisms, and Therapeutic Implications.MedComm · 2025Review
- ECM Remodeling in Direct Inguinal Hernia: The Role of Aging, Oxidative Stress, and Antioxidants Defenses.Clinics and practice · 2025Review
246 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
MicroRNAs (miRNA) are small regulatory RNAs that control gene expression by translational suppression and destabilization of target mRNAs. There is increasing evidence that miRNAs regulate genes associated with fibrosis in organs, such as the heart, kidney, liver, and the lung. In a large-scale screening for miRNAs potentially involved in bleomycin-induced fibrosis, we found expression of miR-29 family members significantly reduced in fibrotic lungs. Analysis of normal lungs showed the presence of miR-29 in subsets of interstitial cells of the alveolar wall, pleura, and at the entrance of the alveolar duct, known sites of pulmonary fibrosis. miR-29 levels inversely correlated with the expression levels of profibrotic target genes and the severity of the fibrosis. To study the impact of miR-29 down-regulation in the lung interstitium, we characterized gene expression profiles of human fetal lung fibroblast IMR-90 cells in which endogenous miR-29 was knocked down. This confirmed the derepression of reported miR-29 targets, including several collagens, but also revealed up-regulation of a large number of previously unrecognized extracellular matrix-associated and remodeling genes. Moreover, we found that miR-29 is suppressed by transforming growth factor (TGF)-β1 in these cells, and that many fibrosis-associated genes up-regulated by TGF-β1 are derepressed by miR-29 knockdown. Interestingly, a comparison of TGF-β1 and miR-29 targets revealed that miR-29 controls an additional subset of fibrosis-related genes, including laminins and integrins, independent of TGF-β1. Together, these strongly suggest a role of miR-29 in the pathogenesis of pulmonary fibrosis. miR-29 may be a potential new therapeutic target for this disease.
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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.