Epigenetic age acceleration and severity of airflow limitation on blood and lung tissue of COPD

Epigenetic Age Acceleration in COPD Blood vs. Lung Tissue

Introduction: Understanding epigenetic age acceleration and severity of airflow limitation on blood and lung tissue of COPD

Accelerated lung aging has been proposed as a mechanism underlying chronic obstructive pulmonary disease (COPD).

The relationship between aging markers in lung tissue and blood of COPD patients and how these markers vary with the severity of airflow limitation remains unclear.

This study explores these questions using DNA methylation-based aging calculation algorithms, known as epigenetic clocks, which are designed to measure the biological age of various tissues.

Methods: DNA Methylation and Epigenetic Clocks

In this study, DNA was extracted from blood (n=168) and lung tissue (n=138) of COPD patients with different degrees of airflow limitation severity (FEV1% ref.).

Genome wide DNA methylation was assessed with EPIC arrays (Illumina), and the biological age and age acceleration was computed with 7 epigenetic clocks, and with the mDNA-TL estimator (a Telomere length shortening measure).

Multivariable linear regressions adjusted for chronological age, sex, pack-year and smoking status, were used for the analysis.

Results: The Impact of Airflow Limitation Severity on Biological Age in COPD Patients

The results showed that in blood, airflow limitation severity was associated with the biological age acceleration determined by three epigenetic clocks (BLUP, Levine, DunedinPACE) and by the mDNA-TL estimator.

By contrast, in lung tissue only the mDNA-TL estimator showed a significant association with the severity of airflow limitation.

Conclusion: Distinct Patterns of Aging Biomarkers in Blood and Lung Tissue of COPD Patients

The findings indicate that COPD patients with more severe airflow limitation present a higher biological epigenetic age acceleration only in blood.

However, both blood and lung tissue of these patients present an accelerated Telomere shortening.

These findings suggest that the pace of aging biomarkers is different in the two tissues.


J. Viglino, S. Casas-Recasen, N. Olvera, T. Garcia, A. Agusti, R. Faner

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