Nitric oxide, free radicals and cell signalling in cardiovascular disease.
Nitric oxide, free radicals and cell signalling in cardiovascular disease.
复制标题
心血管疾病中的一氧化氮、自由基和细胞信号传导。
DOI：
10.1042/bst0250925
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发表时间：
1997
影响因子：
3.9
通讯作者：
White,CR
中科院分区：
文献类型：
--
作者：
Darley-Usmar,VM;McAndrew,J;Patel,R;Moellering,D;Lincoln,TM;Jo,H;Cornwell,T;Digerness,S;White,CR
The modulation of cell signalling by free radicals is an emerging area of vascular research which is providing insight into the orchestration of cell function during complex physiological responses such as inflammation. This is particularly apparent under conditions where defects in signalling pathways are some of the earliest detectable biochemical events. Can free radicals or the oxidants derived from them show the necessary selectivity to inhibit key steps in cellular control mechanisms, despite the fact that components of these pathways are typically at low concentrations relative to other potential targets? Our current understanding of the biology of the free radical NO'sets a precedent, since it clearly satisfies the criteria of potency and selectivity in its role as a messenger molecule [1, 2]. Recent research suggests that this idea may be extended to include the secondary products derived from the reaction of NO'with oxidants produced &a,'+ the inflammatory response [3]. It is proposed that NO and 0;'form reaction products with biological molecules that imitate endogenous second messengers, resulting in changes in the metabolic responses of cells and tissues. The chemically stable free radicals NO'and 0;'react with each other at a rate that is close to that limited by simple diffusion and exceeds that for most other targets in the cell [4]. The product of this reaction, ONOO-, can covalently modify lipids, carbohydrates, nucleic acids and proteins [S-121. It is proposed that these modified biomolecules modulate the inflammatory process through:(1) the formation of lipid mediators;(2) the formation of NO donors;(3) the alteration of Ca2+ sequestration by intracellular organelles such as the mitochondrion, plasma membrane or sarcoplasmic reticulum;(4) modification of cytoskeletal proteins
