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Therapeutic Approach in the Improvement of Endothelial Dysfunction: The Current State of the Art
被引:40
作者:
Radenkovic, Miroslav
[1
]
Stojanovic, Marko
[1
]
Potpara, Tatjana
[2
]
Prostran, Milica
[1
]
机构:
[1] Univ Belgrade, Fac Med, Dept Pharmacol Clin Pharmacol & Toxicol, Belgrade 11129, Serbia
[2] Univ Belgrade, Fac Med, Cardiol Clin, Clin Ctr Serbia, Belgrade 11000, Serbia
关键词:
NITRIC-OXIDE;
SUBCLINICAL HYPOTHYROIDISM;
VASCULAR FUNCTION;
PROGENITOR CELLS;
INFLAMMATION;
ALDOSTERONE;
DISEASE;
SYSTEM;
WOMEN;
GAMMA;
D O I:
10.1155/2013/252158
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:
The endothelium has a central role in the regulation of blood flow through continuous modulation of vascular tone.. is is primarily accomplished by balanced release of endothelial relaxing and contractile factors. The healthy endothelial cells are essential for maintenance of vascular homeostasis involving antioxidant, anti-inflammatory, pro-fibrinolytic, anti-adhesive, or anticoagulant effects. Oppositely, endothelial dysfunction is primarily characterized by impaired regulation of vascular tone as a result of reduced endothelial nitric oxide (NO) synthase activity, lack of cofactors for NO synthesis, attenuated NO release, or increased NO degradation. So far, the pharmacological approach in improving/reversal of endothelial dysfunction was shown to be beneficial in clinical trials that have investigated actions of different cardiovascular drugs. The aim of this paper was to summarize some of the latest clinical findings related to therapeutic possibilities for improving endothelial dysfunction in different pathological conditions. In the majority of presented clinical investigations, the assessment of improvement or reversal of endothelial dysfunction was performed through the flow-mediated dilatation measurement, and in some of those endothelial progenitor cells count was used for the same purpose. Still, given the fast and continuous development of this field, the evidence acquisition included the MEDLINE data base screening and the selection of articles published between 2010 and 2012.
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