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一氧化氮、氧化应激与p66Shc在糖尿病性内皮功能障碍中的相互作用。

Nitric oxide, oxidative stress, and p66Shc interplay in diabetic endothelial dysfunction.

作者信息

Magenta Alessandra, Greco Simona, Capogrossi Maurizio C, Gaetano Carlo, Martelli Fabio

机构信息

Vascular Pathology Laboratory, Istituto Dermopatico dell'Immacolata-IRCCS, 00167 Rome, Italy.

Molecular Cardiology Laboratory, Policlinico San Donato-IRCCS, San Donato Milanese, 20097 Milan, Italy.

出版信息

Biomed Res Int. 2014;2014:193095. doi: 10.1155/2014/193095. Epub 2014 Mar 5.

DOI:10.1155/2014/193095
PMID:24734227
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3964753/
Abstract

Increased oxidative stress and reduced nitric oxide (NO) bioavailability play a causal role in endothelial cell dysfunction occurring in the vasculature of diabetic patients. In this review, we summarized the molecular mechanisms underpinning diabetic endothelial and vascular dysfunction. In particular, we focused our attention on the complex interplay existing among NO, reactive oxygen species (ROS), and one crucial regulator of intracellular ROS production, p66Shc protein.

摘要

氧化应激增加和一氧化氮（NO）生物利用度降低在糖尿病患者血管系统中发生的内皮细胞功能障碍中起因果作用。在本综述中，我们总结了糖尿病内皮和血管功能障碍的分子机制。特别是，我们将注意力集中在NO、活性氧（ROS）和细胞内ROS产生的一个关键调节因子p66Shc蛋白之间存在的复杂相互作用上。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aef8/3964753/eecf05fd41bf/BMRI2014-193095.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aef8/3964753/42ea4bcb9a14/BMRI2014-193095.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aef8/3964753/04f8e1dd2749/BMRI2014-193095.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aef8/3964753/eecf05fd41bf/BMRI2014-193095.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aef8/3964753/42ea4bcb9a14/BMRI2014-193095.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aef8/3964753/04f8e1dd2749/BMRI2014-193095.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aef8/3964753/eecf05fd41bf/BMRI2014-193095.003.jpg

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