摘要
通过心肌细胞内部产生的活性氧和活性氮物种是基本的信号分子,能够调节细胞功能。产生的ROS和RNS精细维持适当的心肌功能,但在许多病理生理条件下会发生改变。因此导致了心肌功能障碍的恶化,最终心力衰竭。事实上,在很多途径中,过量的活性氧和RNS导致心脏肥大,亚硝基-氧化还原反应的平衡的正确调节是EC-偶联机制主要成分发挥功能的基础。因此,提出了广泛的抗氧化治疗改善心肌功能,但这些疗法甚至使生理ROS和RNS信号迟钝,即使有的话,也只能带来有限的益处。另一方面,更有针对性对特定来源或途径的干预措施可能产生不错的效果。
关键词: 心肌肥厚,EC-耦合,心力衰竭,心肌衰弱,活性氮,活性氧
Current Drug Targets
Title:Nitroso-Redox Balance and Modulation of Basal Myocardial Function: An Update from the Italian Society of Cardiovascular Research (SIRC)
Volume: 16 Issue: 8
Author(s): Carlo G. Tocchetti, Marilisa Molinaro, Tommaso Angelone, Vincenzo Lionetti, Rosalinda Madonna, Fabio Mangiacapra, Francesco Moccia, Claudia Penna, Laura Sartiani, Federico Quaini and Pasquale Pagliaro
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关键词: 心肌肥厚,EC-耦合,心力衰竭,心肌衰弱,活性氮,活性氧
摘要: Reactive oxygen species and reactive nitrogen species are produced endogenously by cardiomyocytes and are fundamental signaling molecules that regulate cellular function. Production of ROS and RNS is finely tuned to maintain proper myocardial function, but is altered in many pathophysiological conditions, therefore contributing to worsening myocardial dysfunction and ultimately heart failure. Indeed, an excess of ROS and RNS is central in many pathways leading to cardiac hypertrophy and failure, and the correct regulation of the nitroso-redox balance is fundamental for the function of the main components of the EC-coupling machinery. Broad antioxidant therapies have been proposed to improve myocardial function, but these therapies blunt even physiological ROS and RNS signaling, bringing limited, if any, beneficial effect. On the other hand, more targeted interventions on specific sources or pathways may produce promising results.
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Carlo G. Tocchetti , Marilisa Molinaro , Tommaso Angelone , Vincenzo Lionetti , Rosalinda Madonna , Fabio Mangiacapra , Francesco Moccia , Claudia Penna , Laura Sartiani , Federico Quaini and Pasquale Pagliaro , Nitroso-Redox Balance and Modulation of Basal Myocardial Function: An Update from the Italian Society of Cardiovascular Research (SIRC), Current Drug Targets 2015; 16 (8) . https://dx.doi.org/10.2174/1389450116666150304103517
DOI https://dx.doi.org/10.2174/1389450116666150304103517 |
Print ISSN 1389-4501 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5592 |
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