ITGAV, a specific biomarker associated with the pathogenesis of idiopathic pulmonary fibrosis.

Objective Idiopathic pulmonary fibrosis (IPF), which radiologically/pathologically manifests mainly as usual interstitial pneumonia (UIP), is easily confused with chronic hypersensitivity pneumonitis (CHP) and collagenous vascular disease in clinical settings, affecting the physician's diagnosis and treatment. Accurate identification of IPF from various diseases presenting as UIP is essential for effective diagnosis and therapy. Methods Gene expression data of CHP, IPF, and rheumatoid arthritis-UIP samples were downloaded from the GEO database, and specific biomarkers were identified to differentiate idiopathic UIP/IPF from secondary UIP. We compared gene expression of specific biomarkers between control, secondary UIP, and IPF groups. The mechanism of specific biomarkers in PF was explored by immunohistochemistry, quantitative polymerase chain reaction, immunofluorescence, and flow cytometry. Results We identified integrin alpha V (ITGAV) as a specific biomarker for distinguishing IPF from secondary UIP. We observed a gradual increase in ITGAV expression across the control, secondary UIP, and IPF groups. Animal studies indicated that the elevated expression of ITGAV in various immune cells, particularly in monocyte-derived macrophages, contributed to the development of PF. Conclusion ITGAV is a specific biomarker linked to the pathogenesis of IPF. The identification of ITGAV provides new perspectives for clinical diagnosis, mechanistic studies and new drug development in IPF.