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首页> 外文期刊>Antioxidants and redox signalling >Redox Regulation of Growth and Death in Cardiac Myocytes
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Redox Regulation of Growth and Death in Cardiac Myocytes

机译:心肌细胞生长和死亡的氧化还原调节

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摘要

THIS AND THE NEXT ISSUE OF THE JOURNAL FOCUS On the regulation of myocardial growth and death by reactive oxygen species (ROS) and reactive nitrogen species (RNS), with a special emphasis on cell-signaling mechanisms. During the past decade, a growing number of studies published in peer-reviewed journals have examined the role of oxidative stress in mediating cell growth and death of cardiac myocytes, and the relevance of such mechanisms in cardiac diseases, such as ischemic heart diseases and congestive heart failure. Although oxidative stress has detrimental effects on the heart, such as apoptosisecrosis, fibrosis, cardiac arrhythmia, and mitochondrial dysfunction, it also mediates physiologic and/or protective responses, such as (compensatory) hypertrophy, angiogenesis, and preconditioning effects. The better to illustrate the cardiac role of ROS/RNS, this editorial reviews these contrasting cellular functions of ROS/RNS and their effect on cell-signaling mechanisms
机译:这是和本研究的下一个问题关于活性氧(ROS)和活性氮(RNS)对心肌生长和死亡的调节,特别着重于细胞信号传导机制。在过去的十年中,越来越多的研究在同行评审期刊上发表,研究了氧化应激在介导心肌细胞的细胞生长和死亡中的作用,以及这种机制在心脏病(如缺血性心脏病和充血性心脏病)中的相关性。心脏衰竭。尽管氧化应激会对心脏产生不利影响,例如凋亡/坏死,纤维化,心律不齐和线粒体功能障碍,但它也介导生理和/或保护性反应,例如(代偿性)肥大,血管生成和预处理作用。为了更好地说明ROS / RNS的心脏作用,这篇社论回顾了ROS / RNS的这些相反的细胞功能及其对细胞信号传导机制的影响

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