25-03-2024 | Idiopathic Pulmonary Fibrosis | Brief Report
Identification of non-coding RNA signatures in idiopathic pulmonary fibrosis
Authors:
Alperen Elek, Esra Bozgeyik, Halil Caska, Zekihan Gocer, Ibrahim Bozgeyik
Published in:
Irish Journal of Medical Science (1971 -)
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Abstract
Background
Idiopathic pulmonary fibrosis (IPF) is a deadly, chronic, progressive, irreversible interstitial lung disease characterized by the formation of scar tissue resulting in permanent lung damage. The average survival time following diagnosis is only 3–5 years, with a 5-year survival rate shorter than that of many cancers. Alveolar epithelial cell injury followed by irregular repair is the primary pathological process observed in patients with IPF. An evident characteristic of IPF is the development of fibroblastic foci representing active fibrotic areas. Most of the cells within these foci are believed to be myofibroblasts, which are thought to be the primary source of abnormal extracellular matrix production in IPF. The lung phenotype in IPF is characterized by significantly different processes from healthy lungs, including irregular apoptosis, oxidative stress, and epithelial-mesenchymal transition (EMT) pathways.
Aims
The exact cause of IPF is not fully understood and remains mysterious. It is not suppressing that non-coding RNAs are involved in the development and progression of IPF. Accordingly, here we aimed to identify non-coding RNA molecules during TGFβ-induced myofibroblast activation.
Methods
Differential expression and functional enrichment analysis were employed to reveal the impact of non-coding RNAs during TGFβ-associated lung fibrosis.
Results
Remarkably, LOC101448202, CZ1P-ASNS, LINC01503, IER3-AS1, MIR503HG, CLMAT3, LINC02593, ACTA2-AS1, LOC102723692, LOC107985728, and LOC105371064 were identified to be differentially altered during TGFβ-stimulated myofibroblast activation.
Conclusions
These findings strongly suggest that the mechanism of lung fibrosis is heavily under control of non-coding RNAs, and RNA-based therapies could be a promising approach for future therapeutic interventions to lung fibrosis.