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Strategies to reverse endothelial dysfunction in diabetic nephropathy.逆转糖尿病肾病内皮功能障碍的策略。
Kidney Int. 2012 Dec;82(11):1151-4. doi: 10.1038/ki.2012.306.
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Improvement of endothelial nitric oxide synthase activity retards the progression of diabetic nephropathy in db/db mice.改善内皮型一氧化氮合酶活性可延缓 db/db 小鼠糖尿病肾病的进展。
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Endothelial nitric oxide synthase (eNOS) 4b/a polymorphism and the risk of diabetic nephropathy in type 2 diabetes mellitus: A meta-analysis.内皮型一氧化氮合酶（eNOS）4b/a多态性与2型糖尿病患者糖尿病肾病风险的Meta分析
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本文引用的文献

1
Improvement of endothelial nitric oxide synthase activity retards the progression of diabetic nephropathy in db/db mice.改善内皮型一氧化氮合酶活性可延缓 db/db 小鼠糖尿病肾病的进展。
Kidney Int. 2012 Dec;82(11):1176-83. doi: 10.1038/ki.2012.248. Epub 2012 Jul 11.
2
Diabetic endothelial nitric oxide synthase knockout mice develop advanced diabetic nephropathy.糖尿病内皮型一氧化氮合酶基因敲除小鼠会发展为晚期糖尿病肾病。
J Am Soc Nephrol. 2007 Feb;18(2):539-50. doi: 10.1681/ASN.2006050459. Epub 2007 Jan 3.
3
Endothelial nitric oxide synthase deficiency produces accelerated nephropathy in diabetic mice.内皮型一氧化氮合酶缺乏会加速糖尿病小鼠的肾病进程。
J Am Soc Nephrol. 2006 Oct;17(10):2664-9. doi: 10.1681/ASN.2006070798. Epub 2006 Sep 13.
4
Mechanisms of increased vascular superoxide production in human diabetes mellitus: role of NAD(P)H oxidase and endothelial nitric oxide synthase.人类糖尿病中血管超氧化物生成增加的机制：NAD(P)H氧化酶和内皮型一氧化氮合酶的作用。
Circulation. 2002 Apr 9;105(14):1656-62. doi: 10.1161/01.cir.0000012748.58444.08.
5
The HMG-CoA reductase inhibitor simvastatin activates the protein kinase Akt and promotes angiogenesis in normocholesterolemic animals.HMG-CoA还原酶抑制剂辛伐他汀可激活蛋白激酶Akt，并促进正常胆固醇水平动物的血管生成。
Nat Med. 2000 Sep;6(9):1004-10. doi: 10.1038/79510.
6
Superoxide generation by endothelial nitric oxide synthase: the influence of cofactors.内皮型一氧化氮合酶产生超氧化物：辅助因子的影响。
Proc Natl Acad Sci U S A. 1998 Aug 4;95(16):9220-5. doi: 10.1073/pnas.95.16.9220.
7
Effect of tetrahydrobiopterin on endothelial function in canine middle cerebral arteries.四氢生物蝶呤对犬大脑中动脉内皮功能的影响。
Circ Res. 1996 Aug;79(2):336-42. doi: 10.1161/01.res.79.2.336.
8
Hypertension in mice lacking the gene for endothelial nitric oxide synthase.缺乏内皮型一氧化氮合酶基因的小鼠中的高血压
Nature. 1995 Sep 21;377(6546):239-42. doi: 10.1038/377239a0.
9
Features of endothelial dysfunction in early diabetic nephropathy.早期糖尿病肾病中内皮功能障碍的特征。
Lancet. 1989 Mar 4;1(8636):461-3. doi: 10.1016/s0140-6736(89)91365-2.
10
Increased plasma concentration of von Willebrand factor in insulin dependent diabetics with incipient nephropathy.胰岛素依赖型糖尿病早期肾病患者血浆血管性血友病因子浓度升高。
BMJ. 1989 Jan 7;298(6665):27-8. doi: 10.1136/bmj.298.6665.27-a.

逆转糖尿病肾病内皮功能障碍的策略。

Strategies to reverse endothelial dysfunction in diabetic nephropathy.

机构信息

Division of Nephrology, Baylor College of Medicine, Houston, Texas 77030, USA.

出版信息

Kidney Int. 2012 Dec;82(11):1151-4. doi: 10.1038/ki.2012.306.

DOI:10.1038/ki.2012.306
PMID:23151985
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3914716/
Abstract

Endothelial dysfunction underlies the basic pathophysiology of microvascular complications of diabetes. Endothelial dysfunction is associated with impaired nitric oxide (NO) availability. Since NO production is tightly regulated by endothelial nitric oxide synthase (eNOS), several therapeutic strategies have been investigated and proposed to improve eNOS bioavailability in the vasculature. The findings of Cheng et al. suggest that increased availability of eNOS may be an effective strategy in restoring endothelial function in patients with diabetic nephropathy.

摘要

内皮功能障碍是糖尿病微血管并发症的基本病理生理学基础。内皮功能障碍与一氧化氮（NO）供应受损有关。由于 NO 的产生受到内皮型一氧化氮合酶（eNOS）的严格调节，因此已经研究并提出了几种治疗策略来改善血管中 eNOS 的生物利用度。程等人的研究结果表明，增加 eNOS 的可用性可能是恢复糖尿病肾病患者内皮功能的有效策略。