Saleh Jumana
Jumana Saleh, Department of Biochemistry, College of Medicine and Health Sciences, Sultan Qaboos University, Muscat 123, Oman.
World J Cardiol. 2015 Aug 26;7(8):449-53. doi: 10.4330/wjc.v7.i8.449.
Atherosclerosis is a major complication of diabetes, increasing the risk of cardiovascular related morbidities and mortalities. The hallmark of diabetes is hyperglycemia which duration is best predicted by elevated glycated haemoglobin A1C (HbA1C) levels. Diabetic complications are usually attributed to oxidative stress associated with glycation of major structural and functional proteins. This non-enzymatic glycation of long lived proteins such as collagen, albumin, fibrinogen, liver enzymes and globulins result in the formation of early and advanced glycation end products (AGEs) associated with the production of myriads of free radicles and oxidants that have detrimental effects leading to diabetic complications. AGEs have been extensively discussed in the literature as etiological factors in the advancement of atherogenic events. Mechanisms described include the effects of glycation on protein structure and function that lead to defective receptor binding, impairment of immune system and enzyme function and alteration of basement membrane structural integrity. Hemoglobin (Hb) is a major circulating protein susceptible to glycation. Glycated Hb, namely HbA1C is used as a useful tool in the diagnosis of diabetes progression. Many studies have shown strong positive associations between elevated HbA1C levels and existing cardiovascular disease and major risk factors. Also, several studies presented HbA1C as an independent predictor of cardiovascular risk. In spite of extensive reports on positive associations, limited evidence is available considering the role of glycated Hb in the etiology of atherosclerosis. This editorial highlights potential mechanisms by which glycated hemoglobin may contribute, as a causative factor, to the progression of atherosclerosis in diabetics.
动脉粥样硬化是糖尿病的主要并发症，会增加心血管相关疾病和死亡的风险。糖尿病的标志是高血糖，其持续时间可通过糖化血红蛋白A1C（HbA1C）水平升高得到最佳预测。糖尿病并发症通常归因于与主要结构和功能蛋白糖基化相关的氧化应激。胶原蛋白、白蛋白、纤维蛋白原、肝酶和球蛋白等长寿蛋白的这种非酶糖基化会导致早期和晚期糖基化终产物（AGEs）的形成，这些产物与大量自由基和氧化剂的产生有关，而这些自由基和氧化剂具有有害作用，会导致糖尿病并发症。AGEs作为动脉粥样硬化事件进展的病因学因素在文献中已被广泛讨论。所描述的机制包括糖基化对蛋白质结构和功能的影响，这会导致受体结合缺陷、免疫系统和酶功能受损以及基底膜结构完整性改变。血红蛋白（Hb）是一种易受糖基化影响的主要循环蛋白。糖化血红蛋白，即HbA1C，被用作诊断糖尿病进展的有用工具。许多研究表明，HbA1C水平升高与现有的心血管疾病和主要危险因素之间存在强烈的正相关。此外，多项研究将HbA1C作为心血管风险的独立预测指标。尽管有大量关于正相关的报道，但关于糖化血红蛋白在动脉粥样硬化病因中的作用的证据有限。这篇社论强调了糖化血红蛋白作为一个致病因素可能促进糖尿病患者动脉粥样硬化进展的潜在机制。
