ArticleAmerican journal of respiratory cell and molecular biology2017
miR-34a Inhibits Lung Fibrosis by Inducing Lung Fibroblast Senescence.
Article in American journal of respiratory cell and molecular biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.
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Who cites it
67 citing papers in PubMed, 106 citations in OpenAlex.
- Senolytics in idiopathic pulmonary fibrosis: Results from a first-in-human, open-label, pilot study.EBioMedicine · 2019Trial
- Senotypes define the diverse landscape of senescent cells.Nature aging · 2026Review
- Epigenetic dynamics of cellular senescence: From mechanistic insights to precision senotherapy.Chinese medical journal · 2026Review
- Recent advances on anti-scarring properties of amniotic membrane: emerging strategies and clinical potentials in regenerative medicine.Stem cell research & therapy · 2026Review
- Cadmium exposure triggers vimentin phosphorylation via SIRT6-regulated AKT/PI3K signaling pathway in COPD.European journal of cell biology · 2025Article
- Ubiquitin Specific Protease 9X Regulates the Activation of ARK5 and Promotes Progression of Fibrotic Remodeling.JACC. Basic to translational science · 2025Article
- Therapeutic applications of stem cell-derived exosomes in radiation-induced lung injury.Cancer cell international · 2024Review
- Emerging roles of noncoding RNAs in idiopathic pulmonary fibrosis.Cell death discovery · 2024Review
- The Roles of MicroRNAs in Asthma and Emerging Insights into the Effects of Vitamin DNutrients · 2024Review
- Emerging roles of non-coding RNAs in fibroblast to myofibroblast transition and fibrotic diseases.Frontiers in pharmacology · 2024Review
- [Medical visit status and clinical features in patients with IgG4 related disease].Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences · 2023Article
- [Expression and clinical significance of plasma exosomal miR-34-5p and miR-142-3p in systemic sclerosis].Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences · 2023Article
- Cellular Senescence: A Troy Horse in Pulmonary Fibrosis.International journal of molecular sciences · 2023Review
- Gymnotic uptake of AntimiRs alter microRNA-34a levels in 2D and 3D epithelial cell culture.Molecular therapy. Nucleic acids · 2023Article
- Integrative multi-omics analysis reveals novel idiopathic pulmonary fibrosis endotypes associated with disease progression.Respiratory research · 2023Article
- Construction of a TFs-miRNA-mRNA network related to idiopathic pulmonary fibrosis.Annals of translational medicine · 2023Article
- Senescence-Associated β-Galactosidase Detection in Pathology.Diagnostics (Basel, Switzerland) · 2022Review
- Mechanism of miR-34a in the metabolism of extracellular matrix in fibroblasts of stress urinary incontinence via Nampt-mediated autophagy.Cell stress & chaperones · 2022Article
- Article
- MicroRNA-34a: A Novel Therapeutic Target in Fibrosis.Frontiers in physiology · 2022Review
7 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Cellular senescence has been implicated in diverse pathologies. However, there is conflicting evidence regarding the role of this process in tissue fibrosis. Although dysregulation of microRNAs is a key mechanism in the pathogenesis of lung fibrosis, it is unclear whether microRNAs function by regulating cellular senescence in the disease. In this study, we found that miR-34a demonstrated greater expression in the lungs of patients with idiopathic pulmonary fibrosis and in mice with experimental pulmonary fibrosis, with its primary localization in lung fibroblasts. More importantly, miR-34a was up-regulated significantly in both human and mouse lung myofibroblasts. We found that mice with miR-34a ablation developed more severe pulmonary fibrosis than did wild-type animals after fibrotic lung injury. Mechanistically, we found that miR-34a induced a senescent phenotype in lung fibroblasts because this microRNA increased senescence-associated β-galactosidase activity, enhanced expression of senescence markers, and decreased cell proliferative capacities. Consistently, we found that primary lung fibroblasts from fibrotic lungs of miR-34a-deficient mice had a diminished senescent phenotype and enhanced resistance to apoptosis as compared with those from wild-type animals. We also identified multiple miR-34a targets that likely mediated its activities in inducing senescence in lung fibroblasts. In conclusion, our data suggest that miR-34a functions through a negative feedback mechanism to restrain fibrotic response in the lungs by promoting senescence of pulmonary fibroblasts.
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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.