ArticleScientific reports2016
Loss of miR-140 is a key risk factor for radiation-induced lung fibrosis through reprogramming fibroblasts and macrophages.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 34 citations in OpenAlex.
- Article
- Research progresses on the regulatory roles of microRNAs in radiation-induced pulmonary fibrosis.Journal of molecular histology · 2026Review
- Circular RNA RORβ regulates TGFβR1 in alcohol-induced fibroblast-to-myofibroblast differentiation.Scientific reports · 2025Article
- LncRNA SYISL promotes fibroblast myofibroblast transition via miR-23a-mediated TRIOBP regulation.Cellular and molecular life sciences : CMLS · 2025Article
- Observational
- Noncoding RNAs: Master Regulator of Fibroblast to Myofibroblast Transition in Fibrosis.International journal of molecular sciences · 2023Review
- Tolerogenic dendritic cells in radiation-induced lung injury.Frontiers in immunology · 2023Review
- Lung Pneumonitis and Fibrosis in Cancer Therapy: A Review on Cellular and Molecular Mechanisms.Current drug targets · 2022Review
- Promising Biomarkers of Radiation-Induced Lung Injury: A Review.Biomedicines · 2021Review
- Roles of Macrophage Polarization and Macrophage-Derived miRNAs in Pulmonary Fibrosis.Frontiers in immunology · 2021Review
- NRF2 Regulation by Noncoding RNAs in Cancers: The Present Knowledge and the Way Forward.Cancers · 2020Review
- Harnessing noncoding RNA-based macrophage polarization: Emerging therapeutic opportunities for fibrosis.Immunity, inflammation and disease · 2020Review
- [Research progress on macrophage in radiation induced lung injury].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2020Review
- Microarray analysis of infectious bronchitis virus infection of chicken primary dendritic cells.BMC genomics · 2019Article
- Knockdown of Long Noncoding RNA H19 Represses the Progress of Pulmonary Fibrosis through the Transforming Growth Factor β/Smad3 Pathway by Regulating MicroRNA 140.Molecular and cellular biology · 2019Article
- Advances in Molecular Mechanisms and Treatment of Radiation-Induced Pulmonary Fibrosis.Translational oncology · 2019Review
- Reactive Oxygen Species Drive Epigenetic Changes in Radiation-Induced Fibrosis.Oxidative medicine and cellular longevity · 2019Review
- Impact of miR-140 Deficiency on Non-Alcoholic Fatty Liver Disease.Molecular nutrition & food research · 2018Article
- Comparison of Cardiac miRNA Transcriptomes Induced by Diabetes and Rapamycin Treatment and Identification of a Rapamycin-Associated Cardiac MicroRNA Signature.Oxidative medicine and cellular longevity · 2018Article
- Protective Role of Nuclear Factor-Erythroid 2-Related Factor 2 Against Radiation-Induced Lung Injury and Inflammation.Frontiers in oncology · 2018Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Radiation-induced lung fibrosis (RILF) is a common side effect for patients with thoracic cancer receiving radiation therapy. RILF is characterized by excessive collagen deposition mediated by TGF-β1 and its downstream factor SMAD3, but the exact molecular mechanism leading to fibrosis is yet to be determined. The present study investigated the impact of miR-140 on RILF development. Herein, we first found that loss of miR-140 is a marker of fibrotic lung tissue in vivo one-year post-radiation treatment. We showed that miR-140 knockout primary lung fibroblasts have a higher percentage of myofibroblasts compared to wild type primary lung fibroblasts, and that loss of miR-140 expression leads to increased activation of TGF-β1 signaling as well as increased myofibroblast differentiation. We also identified fibronectin as a novel miR-140 target gene in lung fibroblasts. Finally, we have shown that miR-140 deficiency promotes accumulation of M2 macrophages in irradiated lung tissues. These data suggest that miR-140 is a key protective molecule against RILF through inhibiting myofibroblast differentiation and inflammation.
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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.