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本文引用的文献

1
Vegfa protects the glomerular microvasculature in diabetes.Vegfa 可保护糖尿病患者的肾小球微血管。
Diabetes. 2012 Nov;61(11):2958-66. doi: 10.2337/db11-1655.
2
Wip1-dependent regulation of autophagy, obesity, and atherosclerosis.Wip1 依赖性自噬、肥胖和动脉粥样硬化的调控。
Cell Metab. 2012 Jul 3;16(1):68-80. doi: 10.1016/j.cmet.2012.06.003.
3
Biochemistry, physiology, and pathophysiology of NADPH oxidases in the cardiovascular system.心血管系统中 NADPH 氧化酶的生物化学、生理学和病理生理学。
Circ Res. 2012 May 11;110(10):1364-90. doi: 10.1161/CIRCRESAHA.111.243972.
4
Glomerular VEGF resistance induced by PKCδ/SHP-1 activation and contribution to diabetic nephropathy.肾小球血管内皮生长因子抵抗由蛋白激酶 Cδ/含Src 同源区 2 结构域蛋白酪氨酸磷酸酶 1 激活诱导,并有助于糖尿病肾病发生。
FASEB J. 2012 Jul;26(7):2963-74. doi: 10.1096/fj.11-202994. Epub 2012 Apr 12.
5
Diabetic retinopathy.糖尿病视网膜病变
N Engl J Med. 2012 Mar 29;366(13):1227-39. doi: 10.1056/NEJMra1005073.
6
Macrophage autophagy plays a protective role in advanced atherosclerosis.巨噬细胞自噬在动脉粥样硬化的进展中发挥保护作用。
Cell Metab. 2012 Apr 4;15(4):545-53. doi: 10.1016/j.cmet.2012.01.022. Epub 2012 Mar 22.
7
Protein kinase cβ phosphorylates occludin regulating tight junction trafficking in vascular endothelial growth factor-induced permeability in vivo.蛋白激酶 Cβ磷酸化紧密连接蛋白 occludin 调节血管内皮生长因子诱导的体内通透性的紧密连接转运。
Diabetes. 2012 Jun;61(6):1573-83. doi: 10.2337/db11-1367. Epub 2012 Mar 20.
8
Hyperinsulinemia does not change atherosclerosis development in apolipoprotein E null mice.高胰岛素血症不会改变载脂蛋白 E 基因敲除小鼠的动脉粥样硬化发展。
Arterioscler Thromb Vasc Biol. 2012 May;32(5):1124-31. doi: 10.1161/ATVBAHA.111.239558. Epub 2012 Mar 15.
9
A systems approach identifies HIPK2 as a key regulator of kidney fibrosis.系统方法确定 HIPK2 是肾脏纤维化的关键调节因子。
Nat Med. 2012 Mar 11;18(4):580-8. doi: 10.1038/nm.2685.
10
FoxOs integrate pleiotropic actions of insulin in vascular endothelium to protect mice from atherosclerosis.FoxOs 整合胰岛素在血管内皮中的多效作用,以保护小鼠免受动脉粥样硬化的侵害。
Cell Metab. 2012 Mar 7;15(3):372-81. doi: 10.1016/j.cmet.2012.01.018.

糖尿病的血管并发症:损伤机制和保护因素。

Vascular complications of diabetes: mechanisms of injury and protective factors.

机构信息

Research Division, Joslin Diabetes Center, Boston, MA 02215, USA.

出版信息

Cell Metab. 2013 Jan 8;17(1):20-33. doi: 10.1016/j.cmet.2012.11.012.

DOI:10.1016/j.cmet.2012.11.012
PMID:23312281
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3546345/
Abstract

In patients with diabetes, atherosclerosis is the main reason for impaired life expectancy, and diabetic nephropathy and retinopathy are the largest contributors to end-stage renal disease and blindness, respectively. An improved therapeutic approach to combat diabetic vascular complications might include blocking mechanisms of injury as well as promoting protective or regenerating factors, for example by enhancing the action of insulin-regulated genes in endothelial cells, promoting gene programs leading to induction of antioxidant or anti-inflammatory factors, or improving the sensitivity to vascular cell survival factors. Such strategies could help prevent complications despite suboptimal metabolic control.

摘要

在糖尿病患者中,动脉粥样硬化是导致预期寿命缩短的主要原因,而糖尿病肾病和视网膜病变分别是导致终末期肾病和失明的最大原因。改善治疗方法以对抗糖尿病血管并发症可能包括阻断损伤机制以及促进保护或再生因子,例如通过增强内皮细胞中胰岛素调节基因的作用、促进导致诱导抗氧化或抗炎因子的基因程序,或改善对血管细胞存活因子的敏感性。即使代谢控制不理想,这些策略也有助于预防并发症。