Redox regulation of cardiovascular inflammation - Immunomodulatory function of mitochondrial and Nox-derived reactive oxygen and nitrogen species

被引:123
作者
Wenzel, Philip [1 ,2 ,3 ]
Kossmann, Sabine [1 ,2 ]
Muenzel, Thomas [1 ,2 ,3 ]
Daiber, Andreas [1 ,3 ]
机构
[1] Johannes Gutenberg Univ Mainz, Med Ctr, Ctr Cardiol, Cardiol 1, D-55131 Mainz, Germany
[2] Johannes Gutenberg Univ Mainz, Med Ctr, Ctr Thrombosis & Hemostasis, D-55131 Mainz, Germany
[3] German Ctr Cardiovasc Res DZHK, Partner Site Rhine Main, Mainz, Germany
关键词
Redox regulation; Inflammation; Endothelial dysfunction; ENOS uncoupling; Low-grade inflammation; TOLL-LIKE RECEPTORS; RENIN-ANGIOTENSIN SYSTEM; II-INDUCED HYPERTENSION; NITRIC-OXIDE SYNTHASE; MANGANESE SUPEROXIDE-DISMUTASE; FACTOR-KAPPA-B; HUMAN T-CELLS; OXIDATIVE STRESS; NADPH OXIDASE; ENDOTHELIAL DYSFUNCTION;
D O I
10.1016/j.freeradbiomed.2017.01.027
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Oxidative stress is a major hallmark of cardiovascular diseases although a causal link was so far not proven by large clinical trials. However, there is a close association between oxidative stress and inflammation and increasing evidence for a causal role of (low-grade) inflammation for the onset and progression of cardiovascular diseases, which may serve as the missing link between oxidative stress and cardiovascular morbidity and mortality. With the present review we would like to highlight the multiple redox regulated pathways in inflammation, discuss the sources of reactive oxygen and nitrogen species that are of interest for these processes and finally discuss the importance of angiotensin II (AT-II) as a trigger of cardiovascular inflammation and the initiation and progression of cardiovascular diseases.
引用
收藏
页码:48 / 60
页数:13
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