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Updated: Mar 16, 2026
Refined Murine Model of Idiopathic Pulmonary Fibrosis
Published on: June 17, 2025
MiR-338* suppresses fibrotic pathogenesis in pulmonary fibrosis through targeting LPA1
Yi Zhuang1, Jinghong Dai2, Yongsheng Wang2
1Department of Medical Genetics, Nanjing University School of MedicineNanjing, China; Jiangsu Key Laboratory of Molecular Medicine, Nanjing University School of MedicineNanjing, China; Department of Respiratory Medicine, The Affiliated Drum Tower Hospital of Nanjing University Medical SchoolNanjing, China.
Abstract:
Idiopathic pulmonary fibrosis (IPF) is a progressive lung disease involving pulmonary injury associated with tissue repair, dysfunction and fibrosis. MicroRNAs (miRNAs), as gene regulators, are assumed to regulate about one third of genes and thus play important roles in cellular functions including proliferation, growth, differentiation and apoptosis. Recent studies have indicated that some miRNAs may play critical roles in the pathogenesis of pulmonary fibrosis. In this study, we found that miR-338*(miR-338-5p), which has been found to be associated with tumor progression, was down-regulated in fibroblasts and TGF-β-induced lung fibrotic tissues. Over-expression of miR-338* can partly prevent the fibrotic process induced by TGF-β. Moreover, LPA1 was proven to be a downstream target of miR-338*. Lentivirus-mediated over-expression of miR-338* can alleviate lung fibrosis induced by bleomycin in mice. Taken together, our results suggest that miR-338* attenuates the pathogenesis of pulmonary fibrosis through targeting LPA1. Thus, miR-338* can be a potential therapeutic target for the treatment of IPF.
Insights
MicroRNA-338* (miR-338-5p) is reduced in lung fibrosis. Restoring miR-338* levels may treat idiopathic pulmonary fibrosis by targeting LPA1, offering a potential therapeutic strategy.
Area of Science:
- Biochemistry
- Molecular Biology
- Pulmonary Medicine
Background:
- Idiopathic pulmonary fibrosis (IPF) is a progressive lung disease characterized by lung injury, repair, and fibrosis.
- MicroRNAs (miRNAs) are key gene regulators involved in cellular functions and implicated in pulmonary fibrosis pathogenesis.
Purpose of the Study:
- To investigate the role of miR-338* in the pathogenesis of pulmonary fibrosis.
- To identify potential therapeutic targets for IPF.
Main Methods:
- Quantification of miR-338* in lung fibroblasts and fibrotic tissues.
- Investigating the effect of miR-338* over-expression on TGF-β-induced fibrosis.
- Identifying downstream targets of miR-338*.
- Evaluating the therapeutic potential of lentivirus-mediated miR-338* over-expression in a mouse model of bleomycin-induced lung fibrosis.
Main Results:
- miR-338* was found to be down-regulated in lung fibroblasts and TGF-β-induced fibrotic lung tissues.
- Over-expression of miR-338* partially inhibited the fibrotic process induced by TGF-β.
- LPA1 was identified as a direct downstream target of miR-338*.
- Lentivirus-mediated miR-338* over-expression alleviated bleomycin-induced lung fibrosis in mice.
Conclusions:
- miR-338* plays a protective role in pulmonary fibrosis by targeting LPA1.
- miR-338* represents a potential therapeutic target for treating idiopathic pulmonary fibrosis.
