Accelerated epigenetic ageing after burn injury

Area of Science:

• Biomedical Sciences
• Genetics
• Gerontology

Background:

• Major burn injuries increase the risk of premature age-associated diseases and mortality in survivors.
• The hypothesis that burn injuries accelerate biological aging processes warrants investigation.

Purpose of the Study:

• To investigate the impact of major burn injuries on biological aging using epigenetic clocks.
• To determine if burn injury accelerates epigenetic aging in adult patients.

Main Methods:

• DNA methylation analysis was performed on peripheral blood mononuclear cells from burn-injured patients and healthy controls.
• Epigenetic clocks (PhenoAge, PCGrimAge, Dunedin PACE, Horvath, Hannum) were used to calculate biological age and age acceleration.
• Participants included 53 burn-injured patients (admission and 6-month follow-up) and 29 healthy controls.

Main Results:

• Epigenetic age acceleration was observed at admission, with PhenoAge showing +7.2 years and PCGrimAge +9.23 years.
• Dunedin PACE of aging was 31.65% higher at admission and 11.36% higher at 6 months post-injury compared to controls.
• PCGrimAge remained significantly higher 6 months post-injury, while PhenoAge normalized. Horvath and Hannum clocks showed no significant differences.

Conclusions:

• Burn injury in adults accelerates epigenetic aging, particularly indicated by the Pace of Aging and PCGrimAge.
• This acceleration suggests an increased risk of disease, potentially explaining the higher morbidity and mortality observed in burn survivors.
• While some epigenetic aging markers normalize by 6 months, others persist, highlighting the long-term biological impact of severe burns.