Epigenetic age acceleration in idiopathic pulmonary fibrosis revealed by DNA methylation clocks.

In this research, we delve into the association between epigenetic aging and idiopathic pulmonary fibrosis (IPF), a debilitating lung disease that progresses over time. Utilizing the Illumina MethylationEPIC array, we assessed DNA methylation levels in donated human lung tissue from patients with IPF, categorizing the disease into mild, moderate, and severe stages based on clinical assessments. We used seven epigenetic clocks to determine age acceleration, which is the discrepancy between biological (epigenetic) and chronological age. Our findings revealed a notable acceleration of biological aging in IPF tissues compared with healthy controls, with four clocks-Horvath's, Hannum's, PhenoAge, and DunedinPACE-showing significant correlations. DunedinPACE, in particular, indicated a more rapid aging process in the more severe regions within the lungs of IPF cases. These results suggest that the biological aging process in IPF is expedited and closely tied to the severity of the disease. The study underscores the potential of DNA methylation as a biomarker for IPF, providing valuable insights into the underlying methylation patterns and the dynamics of epigenetic aging in affected lung tissue. This research supports the broader application of epigenetic clocks in clinical prognosis and highlights the critical role of biological age in the context of medical research and healthcare.NEW & NOTEWORTHY Using epigenetic clocks, we found a notable acceleration of biological aging in IPF tissues, particularly in DunedinPACE, suggesting that the biological aging process in IPF is accelerated and closely related to the severity of the disease. The study also underscores DNA methylation's potential as a biomarker for IPF, as well as the dynamics of epigenetic aging and the need to consider biological age in medical research and healthcare.