Dietary advanced glycation end products (AGEs) and their interactions with soluble receptors for advanced glycation end products (sRAGE) play an essential role in the pathogenesis of numerous diseases. RAGE belongs to the immunoglobulin superfamily of receptors that bind several classes of ligands, such as S100/calgranulin family, amyloid β peptides, leukocyte b2 integrin, transthyretin and AGEs. Their production and release cause further interaction with their cell-bound receptor (RAGE), resulting in generation of oxygen radicals, nuclear factor kappa-β, proinflammatory cytokines and cell adhesion molecules. The soluble isoform of receptors for advanced glycation end products acts against the adverse effects of AGE–RAGE interaction by competing with RAGE for binding with AGE. AGEs have been implicated in a number of pathological processes associated not only with micro- and macrovascular disease complications in diabetes, but also in hypertension, cardiovascular disease and atherosclerosis. Low levels of sRAGE have been proposed as biomarkers for many diseases. Evidence acquisition process was performed using PubMed and Medline databases with manually checked articles. A total of 44 articles presenting current knowledge on AGEs, sRAGE and endogenous secretory RAGE (esRAGE), with special focus on their role in the pathogenesis of coronary disease, were reviewed to understand the pathophysiological mechanisms of these receptors. In this review, we discuss structure and function of AGE–RAGE axis in the context of hypertension and cardiovascular diseases.