The role of advanced glycation end-products in the development of coronary artery disease in patients with and without diabetes mellitus: a review.
The role of advanced glycation end-products in the development of coronary artery disease in patients with and without diabetes mellitus: a review.
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DOI：
10.1186/s10020-018-0060-3
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发表时间：
2018-11-23
期刊：
影响因子：
--
通讯作者：
Poretsky L
中科院分区：
文献类型：
--
作者：
Fishman SL;Sonmez H;Basman C;Singh V;Poretsky L
传统的危险因素不足以解释糖尿病 (DM) 患者发生的所有冠状动脉疾病 (CAD) 病例。晚期糖基化终末产物 (AGE) 及其受体可能在 CAD 的发生和进展中发挥重要作用。高血糖是 DM 的标志性特征。随着高血糖持续时间的延长，糖尿病微血管和大血管并发症的发生率也随之增加。即使在实现血糖控制后，这种关联仍然存在，这表明存在“代谢记忆”的先天机制。 AGEs 是糖化蛋白，由于在高血糖情况下产量增加且周转速度通常较慢，因此可以作为代谢记忆的调节剂。 AGE 水平升高会导致细胞外和细胞内蛋白质异常交联，破坏其正常结构和功能。此外，AGE受体的激活可以诱导复杂的信号传导途径，导致炎症增加、氧化应激、钙沉积增加和血管平滑肌细胞凋亡增加，从而导致动脉粥样硬化的发展。通过这些机制，AGEs 可能是 CAD 发展的重要介质。然而，关于 AGE 及其受体在 CAD 进展中的作用的临床研究有限，且结果相互矛盾。 AGE 及其受体可能是判断 CAD 是否存在及其严重程度的有用生物标志物。需要进一步的研究来评估循环和组织 AGE 水平在识别有 CAD 风险的无症状患者或识别可能受益于侵入性干预的患者方面的效用。
Traditional risk factors are insufficient to explain all cases of coronary artery disease (CAD) in patients with diabetes mellitus (DM). Advanced glycation end-products (AGEs) and their receptors may play important roles in the development and progression of CAD. Hyperglycemia is the hallmark feature of DM. An increase in the incidence of both micro-and macrovascular complications of diabetes has been observed with increased duration of hyperglycemia. This association persists even after glycemic control has been achieved, suggesting an innate mechanism of “metabolic memory.” AGEs are glycated proteins that may serve as mediators of metabolic memory due to their increased production in the setting of hyperglycemia and generally slow turnover. Elevated AGE levels can lead to abnormal cross linking of extracellular and intracellular proteins disrupting their normal structure and function. Furthermore, activation of AGE receptors can induce complex signaling pathways leading to increased inflammation, oxidative stress, enhanced calcium deposition, and increased vascular smooth muscle apoptosis, contributing to the development of atherosclerosis. Through these mechanisms, AGEs may be important mediators of the development of CAD. However, clinical studies regarding the role of AGEs and their receptors in advancing CAD are limited, with contradictory results. AGEs and their receptors may be useful biomarkers for the presence and severity of CAD. Further studies are needed to evaluate the utility of circulating and tissue AGE levels in identifying asymptomatic patients at risk for CAD or to identify patients who may benefit from invasive intervention.
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