ArticleInternational journal of molecular sciences2017
miR-1224-5p Mediates Mitochondrial Damage to Affect Silica-Induced Pulmonary Fibrosis by Targeting BECN1.
Article in International journal of molecular sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 31 citations in OpenAlex.
- M2 macrophage-derived apoptotic vesicles alleviate liver fibrosis via miR-1224-5p-mediated inhibition of the SP1/TGF-β pathway in hepatic stellate cells.Journal of nanobiotechnology · 2026Article
- Article
- The emerging role of epigenetic regulation in the progression of silicosis.Clinical epigenetics · 2022Review
- Liposomal UHRF1 siRNA shows lung fibrosis treatment potential through regulation of fibroblast activation.JCI insight · 2022Article
- Pulmonary Toxicity of Silica Linked to Its Micro- or Nanometric Particle Size and Crystal Structure: A Review.Nanomaterials (Basel, Switzerland) · 2022Review
- MicroRNA-205-5p targets E2F1 to promote autophagy and inhibit pulmonary fibrosis in silicosis through impairing SKP2-mediated Beclin1 ubiquitination.Journal of cellular and molecular medicine · 2021Article
- The Mechanism and Effect of Autophagy, Apoptosis, and Pyroptosis on the Progression of Silicosis.International journal of molecular sciences · 2021Review
- Review
- MiR-503 suppresses fibroblast activation and myofibroblast differentiation by targeting VEGFA and FGFR1 in silica-induced pulmonary fibrosis.Journal of cellular and molecular medicine · 2020Article
- Mitochondrial quality control in pulmonary fibrosis.Redox biology · 2020Review
- OGFOD1 negatively regulated by miR-1224-5p promotes proliferation in human papillomavirus-infected laryngeal papillomas.Molecular genetics and genomics : MGG · 2020Article
- MiR-1224-5p Activates Autophagy, Cell Invasion and Inhibits Epithelial-to-Mesenchymal Transition in Osteosarcoma Cells by Directly Targeting PLK1 Through PI3K/AKT/mTOR Signaling Pathway.OncoTargets and therapy · 2020Article
- Mitochondrial dysfunction in fibrotic diseases.Cell death discovery · 2020Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Silicosis is associated with fibroblast proliferation and extracellular matrix deposition in lung tissues. The dysregulation of miR-1224-5p has been implicated in several human cancers; however, the expression and function of miR-1224-5p in silicosis is unknown. The mitochondrial dysfunctions play critical roles in some diseases, but how these processes are regulated in silicosis remains limited. Here, we explored the role of miR-1224-5p in a mouse model of silicosis. We showed that the expression of miR-1224-5p is increased both in lung tissues of silica-induced pulmonary fibrosis and fibroblasts exposed to TGF-β1. Repression of miR-1224-5p expression attenuated silica-induced fibrotic progression in vivo and TGF-β1-induced myofibroblast differentiation in vitro. Additionally, we demonstrated that miR-1224-5p facilitated silica-induced pulmonary fibrosis primarily by repressing one of target genes, BECN1, thereby blocking PARK2 translocation to mitochondria and inducing the accumulation of damaged mitochondria. Furthermore, the activation of PDGFR signal mediated by mitochondrial damage and insufficient mitophagy resulted in myofibroblast differentiation. Collectively, these data indicated that miR-1224-5p exerts key functions in silica-induced pulmonary fibrosis and may represent a potential therapeutic target for silicosis.
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