Researchers identified 4 aging-associated genes that might be involved in the development of pulmonary fibrosis.
The genes were identified through data mining of gene expression profiles from patients with idiopathic pulmonary fibrosis (IPF) and a mouse model with bleomycin-induced pulmonary fibrosis (BIPF).
“Aging is a strong risk factor and an independent prognostic biomarker for progressive IPF. However, a comprehensive analysis based on gene expression profiles for the investigation of the role played by aging in IPF was missing,” the authors said in the study published in Frontiers in Medicine.
Continue Reading
The 4 core genes identified in this study were expressed differently in both patients with IPF and BIPF mice datasets. These included solute carrier family 2 member 3 (Slc2a3), fibrinogen alpha chain (Fga), haptoglobin (Hp), and thrombospondin 1 (Thbs1).
To validate the changes in the expression of the 4 core genes identified via bioinformatics, Lu et al evaluated their expression in young and aged mice with or without the disease. The results showed that Slc2a3 and Fga increased with age in both BIPF and control mice, while Hp and Thbs1 decreased with age.
Read more about IPF complications
Other studies have addressed the role of these genes and the potential impact on the pathogenesis of IPF.
Slc2a3 mediates the uptake of various monosaccharides. Variations in Slc2a3 transcription levels might be associated with inflammation. Fga is involved in the formation of the insoluble fibrin matrix.
Fga is overexpressed in patients with IPF when compared to healthy controls and the lack of a C-terminal fragment in its structure has been linked with the progress of fibrosis in patients with liver diseases.
Hp is important for the renewal of type 2 alveolar epithelial cells. It mediates lung repair and delays the development of fibrosis. Thbs1 is involved in matrix homeostasis.
Reference
Lu Y, Chen J, Wang S, et al. Identification of genetic signature associated with aging in pulmonary fibrosis. Front Med. 2021;8:1866. doi:10.3389/fmed.2021.744239
