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AI-driven toolset for IPF and aging research associates lung fibrosis with accelerated aging

2025/08/08 by Fedor Galkin, Shan Chen, Alexander Aliper +2 · 1 voice · 1 citation
Immunology and Microbiology · Medicine · #IL-33, ST2, and ILC Pathways #Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis #Systemic Sclerosis and Related Diseases

paper · pdf · doi:10.18632/aging.206295

openalex publication_date 2025/08/08 · openalex created_date 2025/10/10 · openalex updated_date 2026/07/30

Abstract

Idiopathic pulmonary fibrosis (IPF) is a condition predominantly affecting the elderly and leading to a decline in lung function. Our study investigates the aging-related mechanisms in IPF using artificial intelligence (AI) approaches. We developed a pathway-aware proteomic aging clock using UK Biobank data and applied it alongside a specialized version of Precious3GPT (ipf-P3GPT) to demonstrate an AI-driven mode of IPF research. The aging clock shows great performance in cross-validation (R2=0.84) and its utility is validated in an independent dataset to show that severe cases of COVID-19 are associated with an increased aging rate. Computational analysis using ipf-P3GPT revealed distinct but overlapping molecular signatures between aging and IPF, suggesting that IPF represents a dysregulation rather than mere acceleration of normal aging processes. Our findings establish novel connections between aging biology and IPF pathogenesis while demonstrating the potential of AI-guided approaches in therapeutic development for age-related diseases.

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