Diabetes mellitus is a chronic disease caused by a deficiency in the production of insulin and/or by the effects of insulin resistance. Insulin deficiency leads to hyperglycemia which is the major initiator of diabetic cardiovascular complications escalating with time and driven by many complex biochemical and molecular processes. Four hypotheses, which propose mechanisms of diabetes-associated pathophysiology, are currently considered. Cardiovascular impairment may be caused by an increase in polyol pathway flux, by intracellular advanced glycation end-products formation or increased flux through the hexosamine pathway. The latter of these mechanisms involves activation of the protein kinase C. Cellular and mitochondrial metabolism alterations observed in the course of diabetes are partially associated with an excessive production of reactive oxygen species (ROS). Among many processes and factors involved in ROS production, the 66 kDa isoform of the growth factor adaptor shc (p66Shc protein) is of particular interest. This protein plays a key role in the control of mitochondria-dependent oxidative balance thus it involvement in diabetic complications and other oxidative stress based pathologies is recently intensively studied. In this review we summarize the current understanding of hyperglycemia induced cardiac mitochondrial dysfunction with an emphasis on the oxidative stress and p66Shc protein. This article is part of a Directed Issue entitled: Bioenergetic dysfunction, adaptation and therapy.

译文

糖尿病是由胰岛素产生不足和/或胰岛素抵抗的影响引起的慢性疾病。胰岛素缺乏导致高血糖,高血糖是糖尿病心血管并发症的主要诱因,并由许多复杂的生化和分子过程驱动。目前考虑了四个假设,这些假设提出了与糖尿病相关的病理生理学机制。心血管损害可能是由多元醇途径通量的增加,细胞内晚期糖基化终产物的形成或通过己糖胺途径的通量增加引起的。这些机制中的后者涉及蛋白激酶C的激活。在糖尿病过程中观察到的细胞和线粒体代谢变化部分与活性氧 (ROS) 的过量产生有关。在涉及ROS生产的许多过程和因素中,生长因子衔接子shc (p66Shc蛋白) 的66 kDa同工型特别令人感兴趣。该蛋白在控制线粒体依赖性氧化平衡中起关键作用,因此最近对其参与糖尿病并发症和其他基于氧化应激的病理进行了深入研究。在这篇综述中,我们总结了目前对高血糖诱导的心脏线粒体功能障碍的理解,重点是氧化应激和p66Shc蛋白。本文是题为 “生物能功能障碍,适应和治疗” 的定向问题的一部分。

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