The roles of advanced glycation end products in cardiovascular diseases: from mechanisms to therapeutic strategies

Abstract

Advanced glycation end products (AGEs) are deleterious to tissues in vivo, arising from the process of non-enzymatic glycation (NEG), also referred to as the Maillard Reaction, which facilitates the non-enzymatic modification of biomolecules by saccharides. AGEs are integral to the physiological and pathophysiological processes associated with senescence, cardiovascular diseases (CVDs), neurodegenerative and neuroinflammatory diseases, diabetes mellitus (DM) and its complications, autoimmune and rheumatic inflammatory diseases, bone-degenerative diseases, and chronic renal diseases. Both endogenous AGEs and exogenous dietary AGEs can affect the structures and functions of proteins and lipids in cardiovascular tissues and the extracellular matrix of cardiovascular cells by inducing oxidative stress and inflammatory responses, causing direct cell and tissue dysfunction, and activating subsequent signaling pathways mediated by the AGE-RAGE axis. This review focuses on the roles and mechanisms of AGEs in CVDs, from cardiovascular tissues to concrete diseases like heart failure, valvular heart disease, and so on, together with the corresponding treatment and prevention strategies, aiming to provide a comprehensive overview of the roles of AGEs in CVDs and corresponding therapeutic measures.