Why the study?
In diabetic metabolic disorders, advanced glycation end products contribute significantly to the development of cardiovascular diseases, but the molecular mechanisms underlying AGE-mediated vascular injury required comprehensive elucidation.
This review highlights the molecular mechanisms of AGE-mediated vascular injury and potential therapeutic strategies for CVD prevention in diabetic patients.
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AGE-targeted therapies should not yet alter diabetic CVD care; leaves open need for RCTs to test efficacy.
BACKGROUND: In diabetic metabolic disorders, advanced glycation end products (AGEs) contribute significantly to the development of cardiovascular diseases (CVD). AIMS: This comprehensive review aims to elucidate the molecular mechanisms underlying AGE-mediated vascular injury. CONCLUSIONS: We discuss the formation and accumulation of AGEs, their interactions with cellular receptors, and the subsequent activation of signaling pathways leading to oxidative stress, inflammation, endothelial dysfunction, smooth muscle cell proliferation, extracellular matrix remodeling, and impaired angiogenesis. Moreover, we explore potential therapeutic strategies targeting AGEs and related pathways for CVD prevention and treatment in diabetic metabolic disorders. Finally, we address current challenges and future directions in the field, emphasizing the importance of understanding the molecular links between AGEs and vascular injury to improve patient outcomes.
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Liu et al. (2023) studied this question.
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