Receptor for Advanced Glycation End Products in Cardiovascular and Diabetic Complication(s)

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The Receptor for Advanced Glycation End Products (RAGE) has emerged as a pivotal player in the pathogenesis of cardiovascular and diabetic complications. An in-depth exploration of RAGE involvement in the disease processes, elucidating the molecular mechanisms, signaling pathways, and the associated pathological outcomes, is discussed. In diabetes, chronic hyperglycemia leads to the formation and accumulation of advanced glycation end products (AGEs), which activate RAGE and subsequently initiate a cascade of pro-inflammatory and pro-oxidative events. These processes contribute to the development and progression of diabetic vascular complications, including atherosclerosis, neuropathy, nephropathy, and retinopathy. In the cardiovascular system, RAGE activation promotes vascular inflammation, endothelial dysfunction, and vascular smooth muscle cell proliferation, all of which are critical in the pathogenesis of atherosclerosis and cardiovascular diseases. Furthermore, RAGE-mediated oxidative stress and inflammation have been implicated in the progression of heart failure and post-ischemic injury. Targeting RAGE signaling thereby emerges as a promising therapeutic approach to mitigate the detrimental effects of chronic hyperglycemia and vascular inflammation in diabetic and cardiovascular diseases. A comprehensive understanding of the multifaceted RAGE functions in cardiovascular complications such as atherosclerosis, peripheral arterial disease, atrial fibrillation, thrombotic disorder, myocardial infarction, vascular calcification, and the role of RAGE in diabetes-associated cardiac fibrosis, is discussed with a focus on therapeutic significance.