Epigenetic age acceleration in diabetes and its clinical implications.
Abstract
Epigenetic age acceleration (EAA), a discrepancy between biological and chronological age based on DNA methylation patterns, has emerged as a critical marker for aging and metabolic health. Individuals with diabetes, particularly type 2 diabetes (T2D), exhibit notable EAA, linking the disease to accelerated biological ageing. This review explores the mechanisms underlying EAA in diabetes, including hyperglycaemia-induced oxidative stress, inflammation, and dysregulated epigenetic pathways. Additionally, we discuss the clinical implications of EAA, emphasizing its potential as a biomarker for diabetes-related complications and a predictor of cardiovascular disease, nephropathy, and premature mortality. Emerging therapeutic strategies targeting epigenetic mechanisms, such as dietary interventions, pharmacological agents, and lifestyle modifications, are also reviewed. Understanding the interplay between EAA and diabetes opens avenues for personalized medicine and innovative treatments aimed at mitigating the accelerated aging phenotype associated with diabetes.
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Research summary
Epigenetic age acceleration in individuals with diabetes serves as a potential biomarker for diabetes-related complications and accelerated biological aging. The paper is relevant as it explores mechanisms linking diabetes to accelerated aging, which could inform strategies for longevity and age-related disease management.
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