ArticleScientific reports2017
The role of miR-497-5p in myofibroblast differentiation of LR-MSCs and pulmonary fibrogenesis.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 48 citations in OpenAlex.
- SIRT3-mediated deacetylation of FoxM1 prevents pulmonary fibrosis via modulating the activation of pulmonary fibroblasts.Redox biology · 2026Article
- Interleukin 11-Induced MicroRNAs as Functional Mediators and Circulating Biomarkers of Cardiac Fibrosis.Circulation research · 2026Article
- MiR-497-5p Ameliorates Deep Venous Thrombosis by Facilitating Endothelial Progenitor Cell Migration and Angiogenesis by Regulating LITAF.Biochemical genetics · 2025Article
- Review
- Bone marrow mesenchymal stem cells-derived exosomes promote spinal cord injury repair through the miR-497-5p/TXNIP/NLRP3 axis.Journal of molecular histology · 2024Article
- Article
- Emerging roles of non-coding RNAs in fibroblast to myofibroblast transition and fibrotic diseases.Frontiers in pharmacology · 2024Review
- Tetramethylpyrazine promotes angiogenesis and nerve regeneration and nerve defect repair in rats with spinal cord injury.Heliyon · 2023Article
- Super Carbonate Apatite-miR-497a-5p Complex Is a Promising Therapeutic Option against Inflammatory Bowel Disease.Pharmaceuticals (Basel, Switzerland) · 2023Article
- Pulmonary endogenous progenitor stem cell subpopulation: Physiology, pathogenesis, and progress.Journal of intensive medicine · 2023Review
- Boosting therapeutic efficacy of mesenchymal stem cells in pulmonary fibrosis: The role of genetic modification and preconditioning strategies.Iranian journal of basic medical sciences · 2023Review
- Inhibition of miR-497 Attenuates Oral Submucous Fibrosis by Inhibiting Myofibroblast Transdifferentiation in Buccal Mucosal Fibroblasts.Oral health & preventive dentistry · 2022Article
- Current and prospective applications of exosomal microRNAs in pulmonary fibrosis (Review).International journal of molecular medicine · 2022Review
- Serum microRNAs in osteoporotic fracture and osteoarthritis: a genetic and functional study.Scientific reports · 2021Article
- Macrophage activation in the lung during the progression of nitrogen mustard induced injury is associated with histone modifications and altered miRNA expression.Toxicology and applied pharmacology · 2021Article
- Reversion inducing cysteine rich protein with Kazal motifs and cardiovascular diseases: The RECKlessness of adverse remodeling.Cellular signalling · 2021Review
- MicroRNA-497-5p downregulation inhibits cell viability, reduces extracellular matrix deposition and induces apoptosis in human hyperplastic scar fibroblasts by regulating Smad7.Experimental and therapeutic medicine · 2021Article
- The function of non-coding RNAs in idiopathic pulmonary fibrosis.Open medicine (Warsaw, Poland) · 2021Review
- Regulatory Immune Cells in Idiopathic Pulmonary Fibrosis: Friends or Foes?Frontiers in immunology · 2021Review
- Inhibition of miR-497-3p Downregulates the Expression of Procalcitonin and Ameliorates Bacterial Pneumonia in Mice.Inflammation · 2020Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 3 countries.
Funding
Abstract
Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive and fatal fibrotic lung disease characterized by profound changes in stem cell differentiation, epithelial cell phenotypes and fibroblast proliferation. In our study, we found that miR-497-5p was significantly upregulated both during myofibroblast differentiation of lung resident mesenchymal stem cells (LR-MSCs) and in the lung tissues of a pulmonary fibrosis model. In addition, as determined by luciferase assays and Western blot analysis, reversion-inducing cysteine-rich protein with kazal motifs (Reck) was identified to be one of the target genes of miR-497-5p, and Reck could suppress the expression of matrix metalloproteinase-2 (Mmp2) and Mmp9, which could activate latent transforming growth factor-β1 (TGF-β1). To test the potential therapeutic significance of this miRNA, we modulated the expression of miR-497-5p in LR-MSCs and relevant animal models. The results demonstrated that upregulation of miR-497-5p could induce LR-MSCs to differentiate into myofibroblasts and promote pulmonary fibrogenesis, while inhibition of its expression could effectively retard these processes. In conclusion, our work supports that controlling pulmonary fibrogenesis via inhibition of miR-497-5p expression may provide a potential therapeutic strategy for 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.