醛糖还原酶在糖尿病视网膜病变中作用的研究进展
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国家自然科学基金项目(No.81260153); 云南省应用基础研究计划自筹经费项目(No.2011FZ162)


Research progress on the roles of aldose reductase in diabetic retinopathy
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National Natural Foundation of China(No.81260153); Yunnan Applied Basic Research Program of Self-financing Project(No.2011FZ162)

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    摘要:

    醛糖还原酶(aldose reductase,AR)属于烟酰胺腺嘌呤二核苷酸(nicotinamide-adenine dinudeotide phosphate,NADPH)依赖性的醛-酮还原酶超家族,是多元醇代谢通路中的关键限速酶,在机体高糖代谢中发挥重要作用。AR广泛存在于肾脏、血管、晶状体、视网膜、心脏、骨骼肌等组织器官中,催化葡萄糖转化为不易通透细胞膜的山梨醇,使细胞肿胀、变性、坏死,与糖尿病慢性并发症的发生发展有密切关系。糖尿病视网膜病变(diabetic retinopathy,DR)为多因素疾病,目前确切的病因尚不清楚,但多元醇代谢通路被证实在DR发病机制中发挥重要作用。临床工作中控制血糖、血压等危险因素的治疗方案对于DR的病情缓解仅有部分疗效或无效,如果能明确与DR病情相关的基因,将有助于更好地理解其病理机制,有助于新治疗方法及药物的研制。本文就目前AR及其基因多态性在DR中的作用和AR抑制剂的临床应用进行综述。

    Abstract:

    Aldose reductase(AR)belonging to nicotinamide-adenine dinucleotide phosphate(NADPH)-dependent aldehyde-keto reductase superfamily, is the key rate-limiting enzyme in the polyol pathway which plays an important role in the body's high-sugar metabolism. AR is widely present in the kidneys, blood vessels, lens, retina, heart, skeletal muscle and other tissues and organs, converts glucose to sorbitol which easy permeability of cell membranes, cause cell swelling, degeneration, necrosis, and have a close relationship with the development of chronic complications of diabetes mellitus. Diabetic retinopathy(DR)is a multifactorial disease, the exact cause is currently unknown, but polyol pathway has been demonstrated to play an important role in the pathogenesis of DR. Clinical risk factors such as blood sugar control, blood pressure and other treatments for DR only play a part effect of remission or invalid, if we can find out DR genes associated with the disease, this will contribute to a better understanding of the pathological mechanisms and contribute to the development of new treatments and drugs. The current research progress of AR, AR gene polymorphism, Aldose reductase inhibitors to DR was reviewed in this article.

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李宏哲,李才锐,孙曙光.醛糖还原酶在糖尿病视网膜病变中作用的研究进展.国际眼科杂志, 2015,15(7):1176-1178.

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  • 收稿日期:2015-04-07
  • 最后修改日期:2015-06-04
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  • 在线发布日期: 2015-07-01
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