Nitric Oxide, Oxidative Stress, and p66Shc Interplay in Diabetic Endothelial Dysfunction

被引:95
|
作者
Magenta, Alessandra [1 ]
Greco, Simona [2 ]
Capogrossi, Maurizio C. [1 ]
Gaetano, Carlo [3 ]
Martelli, Fabio [2 ]
机构
[1] Ist Dermopat Immacolata IRCCS, Vasc Pathol Lab, I-00167 Rome, Italy
[2] Policlin San Donato IRCCS, Mol Cardiol Lab, I-20097 Milan, Italy
[3] Goethe Univ Frankfurt, Div Cardiovasc Epigenet, Dept Cardiol, Internal Med Clin 3, D-60590 Frankfurt, Germany
关键词
LIFE-SPAN DETERMINANT; INFLAMMATORY GENE-EXPRESSION; FOXO TRANSCRIPTION FACTORS; SMOOTH-MUSCLE-CELLS; C-REACTIVE PROTEIN; NF-KAPPA-B; INSULIN-RESISTANCE; ADAPTER PROTEIN; SKELETAL-MUSCLE; MATERNAL-HYPERCHOLESTEROLEMIA;
D O I
10.1155/2014/193095
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
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, p66(Shc) protein.
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页数:16
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