ArticleScientific reports2016
miR-489 inhibits silica-induced pulmonary fibrosis by targeting MyD88 and Smad3 and is negatively regulated by lncRNA CHRF.
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 54 papers.
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Who cites it
54 citing papers in PubMed, 100 citations in OpenAlex.
- Profibrotic macrophage populations and cell communications in pulmonary fibrosis.Journal of physiology and biochemistry · 2026Review
- LncRNA CHRF: molecular mechanisms and therapeutic potentials in cardiovascular diseases, cancers and fibrosis.Frontiers in cell and developmental biology · 2025Review
- Roles of lncRNAs in NF-κB-Mediated Macrophage Inflammation and Their Implications in the Pathogenesis of Human Diseases.International journal of molecular sciences · 2024Review
- Ginsenoside Re inhibits myocardial fibrosis by regulating miR-489/myd88/NF-κB pathway.Journal of ginseng research · 2023Article
- Long noncoding RNA MyD88 functions as a promising diagnostic biomarker in hepatocellular carcinoma.Frontiers in endocrinology · 2023Article
- The emerging role of epigenetic regulation in the progression of silicosis.Clinical epigenetics · 2022Review
- Long Non-Coding RNAs in Cardiac and Pulmonary Fibroblasts and Fibrosis.Non-coding RNA · 2022Article
- Downregulation of lncRNA Miat contributes to the protective effect of electroacupuncture against myocardial fibrosis.Chinese medicine · 2022Article
- Article
- Long non-coding RNA HCG18 promotes gastric cancer progression by regulating miRNA-146a-5p/tumor necrosis factor receptor-associated factor 6 axis.Bioengineered · 2022Article
- IL-1β-Triggered Long Non-coding RNA CHRF Induces Non-Small Cell Lung Cancer by Modulating the microRNA-489/Myd88 Axis.Journal of Cancer · 2022Article
- The single nucleotide polymorphism rs1814521 in long non-coding RNA ADGRG3 associates with the susceptibility to silicosis: a multi-stage study.Environmental health and preventive medicine · 2022Article
- SIS3 Alleviates Cisplatin-Induced Acute Kidney Injury by Regulating the LncRNA Arid2-IR-Transferrin Receptor Pathway.Kidney & blood pressure research · 2022Article
- Epigenetic Changes and Functions in Pneumoconiosis.Oxidative medicine and cellular longevity · 2022Review
- Review
- miR-489-3p overexpression inhibits lipopolysaccharide-induced nucleus pulposus cell apoptosis, inflammation and extracellular matrix degradation via targeting Toll-like receptor 4.Experimental and therapeutic medicine · 2021Article
- A novel inactivated whole-cell Pseudomonas aeruginosa vaccine that acts through the cGAS-STING pathway.Signal transduction and targeted therapy · 2021Article
- Long Noncoding RNAInternational journal of molecular sciences · 2021Article
- Dynamic assessing silica particle-induced pulmonary fibrosis and associated regulation of long non-coding RNA expression in Wistar rats.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2021Article
- Dexmedetomidine suppresses bupivacaine-induced parthanatos in human SH-SY5Y cells via the miR-7-5p/PARP1 axis-mediated ROS.Naunyn-Schmiedeberg's archives of pharmacology · 2021Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Silicosis is an incurable occupational disease associated with inflammation, fibroblast proliferation and the accumulation of extracellular matrix in lung tissues. The dysregulation of lncRNAs and miRNAs has been implicated in many complex diseases; however, the current understanding of their roles in fibrotic lung diseases, especially silicosis, remains limited. Our previous microRNA (miRNA, miR) microarray data have indicated decreased expression levels of miR-489 in lung tissues of silica-induced pulmonary fibrosis. Here, we further explored the role of miR-489 in a mouse model of silicosis. Interestingly, miR-489 levels were reduced in both macrophages that were exposed to silica and fibroblasts that were exposed to TGF-β1. Additionally, the overexpressed miR-489 carried out its anti-fibrotic role by attenuating inflammation and fibrotic progression in vivo. Our molecular study further demonstrated that miR-489 inhibited silica-induced pulmonary fibrosis primarily by repressing its target genes MyD88 and Smad3. Moreover, the up-regulated lncRNA cardiac hypertrophy-related factor (CHRF) reversed the inhibitory effect of miR-489 on MyD88 and Smad3 and then triggered the inflammation and fibrotic signaling pathways. Overall, our data indicate that the CHRF-miR-489-MyD88 Smad3 signaling axis exerts key functions in silica-induced pulmonary fibrosis and may represent a therapeutic target for silicosis.
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