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Updated: Apr 16, 2026
Refined Murine Model of Idiopathic Pulmonary Fibrosis
Published on: June 17, 2025
Discovery and validation of extracellular/circulating microRNAs during idiopathic pulmonary fibrosis disease
Guanghai Yang1, Lin Yang2, Wendong Wang1
1Department of Thoracic Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, Hubei Province, China.
Background:
Idiopathic pulmonary fibrosis (IPF) is a chronic fibrosing interstitial lung disease of unknown etiology that is currently untreatable. In this study we aim to characterize the potential of extracellular/circulating microRNAs (miRNAs) in serum as biomarkers for IPF.
Methods:
Total serum RNAs were isolated from serum from healthy control subjects (n=12), rapid progressive (n=12) and slowly progressive IPF patients (n=12). Serum RNA was analyzed by using TaqMan microRNA assays containing probes for 366 human miRNAs, and selected findings were validated with quantitative RT-PCR. Target prediction and pathway analysis on the significant differential miRNAs were performed using DIANA-mirPath.
Results:
We found 47 significantly differentially expressed serum miRNAs (p<0.05) in rapid progressive or slowly progressive IPF patients compared to healthy controls, including 21 up-regulated miRNAs and 26 down-regulated miRNAs. Bioinformatic analysis by DIANA-mirPath demonstrated that 53 KEGG biological processes were significantly enriched (p < 0.05, FDR corrected) among differentially expressed serum miRNAs, including TGF-beta signaling pathway (p < 0.0001), MAPK signaling pathway (p < 0.0001), PI3K-Akt signaling pathway (p < 0.0001), Wnt signaling pathway (p < 0.0001), HIF-1 signaling pathway (p < 0.0001), Regulation of actin cytoskeleton (p < 0.0001), Jak-STAT signaling pathway (p < 0.0001), Notch signaling pathway (p < 0.0001), and Cytokine-cytokine receptor interaction (p = 0.0062). We further validated six miRNAs (miR-21, miR-199a-5p, miR-200c, miR-31, let-7a, and let-7d) for further validation using an independent cohort of 20 rapid progressive IPF, 24 slowly progressive IPF patients and 20 healthy controls. In agreement with the preliminary data from miRNA assay, miR-21, miR-199a-5p, and miR-200c were significantly increased in serums of IPF patients while miR-31, let-7a, and let-7d were significantly under expressed in serums of IPF patients compared to healthy controls.
Conclusions:
These studies demonstrated that extracellular/circulating miRNAs in serum could be potentially served as novel regulators influencing disease progression of IPF.
Insights
Extracellular microRNAs (miRNAs) in serum show potential as biomarkers for idiopathic pulmonary fibrosis (IPF). This study identified 47 differentially expressed miRNAs, offering new insights into IPF progression and potential therapeutic targets.
Area of Science:
- Pulmonary Medicine
- Molecular Biology
- Biomarker Discovery
Background:
- Idiopathic pulmonary fibrosis (IPF) is a progressive, untreatable lung disease.
- The etiology of IPF remains unknown.
- Extracellular/circulating microRNAs (miRNAs) are investigated as potential biomarkers for IPF.
Purpose of the Study:
- To characterize circulating miRNAs in serum as potential biomarkers for IPF.
- To identify differentially expressed miRNAs in IPF patients compared to healthy controls.
Main Methods:
- Serum RNA isolation from IPF patients and healthy controls.
- TaqMan miRNA assays to analyze 366 human miRNAs.
- Quantitative RT-PCR for validation and DIANA-mirPath for pathway analysis.
Main Results:
- 47 significantly differentially expressed serum miRNAs identified (p<0.05).
- Enrichment analysis revealed involvement of key signaling pathways (e.g., TGF-beta, MAPK, PI3K-Akt).
- Six miRNAs (miR-21, miR-199a-5p, miR-200c, miR-31, let-7a, let-7d) validated in an independent cohort.
Conclusions:
- Circulating miRNAs in serum show potential as novel biomarkers for IPF.
- These miRNAs may act as regulators influencing IPF disease progression.
- Further research into miRNA-based diagnostics and therapeutics for IPF is warranted.
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