Abstract

Advanced glycation end products (AGEs) are a heterogeneous group of compounds formed during the advanced stages of the Maillard reaction through non-enzymatic reactions, occurring mainly between reducing sugars or their oxidation metabolites and amino groups in proteins, lipids, and nucleic acids. These compounds can be endogenously formed, particularly under hyperglycemic conditions. In addition, AGEs are also produced exogenously during the thermal processing of foods, contributing to the dietary intake of these compounds. The accumulation of AGEs in body tissues has been associated with aging and the pathogenesis of various non-communicable diseases. Dietary intake of AGEs contributes significantly to their systemic burden. Consequently, reducing the intake of dietary AGEs has been proposed as a modifiable risk factor for the prevention of chronic, age-related diseases. This review examines and discusses current evidence on the molecular mechanisms by which dietary and endogenous AGEs contribute to cellular senescence and the progression of prevalent age-associated pathologies, including diabetes, cardiovascular diseases, musculoskeletal disorders, and neurodegeneration. © 2025 Elsevier B.V. and Société Française de Biochimie et Biologie Moléculaire (SFBBM)