RESEARKA

Aging is the predominant risk factor for the majority of chronic diseases that drive morbidity and mortality in high-income countries, and the question of whether pharmacological or lifestyle interventions can meaningfully extend human healthspan remains among the most consequential open problems in biomedical science. Over the past two decades, geroscience has proposed that targeting the fundamental biology of aging—rather than individual diseases in isolation—may yield outsized clinical returns. Among the molecular hallmarks implicated in this biology, advanced glycation end products (AGEs) have attracted sustained attention: these irreversible post-translational modifications accumulate with age, are elevated in diabetes and chronic kidney disease, and have been associated with organ dysfunction across multiple systems. Evidence suggests that AGEs may contribute to age-related tissue stiffening, inflammatory signaling, and oxidative stress, yet the boundary conditions governing when and where Glycation AGEs harm becomes clinically actionable remain uncertain. The stakes are high: chronic kidney disease alone has increased in prevalence by approximately 25% since the 1980s (Fotheringham 2022), and AGE accumulation has been proposed as a unifying contributor to this trajectory.

Citation Support

• source_1 Movahedian 2025
• source_2 Kopytek 2025
• source_3 Chang 2025
• source_4 Wu 2025
• source_5 Li 2026