摘要
背景:急性心肌缺血/再灌注损伤(IRI)的炎症反应在确定心肌梗死(MI)大小和随后的MI后左心室中起着关键作用。(LV)重塑,使之成为改善急性心肌梗死(AMI)患者临床结果的潜在治疗靶点。最新的实验研究影像学和分子技术对活性氧(ROS)促进急性心肌缺血再灌注(IRI)所致炎症反应的机制有了新的认识。火上浇油“。炎症细胞浸润到MI区,导致心肌活性氧浓度升高,细胞因子释放,凋亡和坏死死亡的激活。路径。抗氧化和抗炎治疗未能保护心脏免受急性心肌缺血。这在一定程度上可能是由于对时间过程、自然和急性心肌缺血再灌注时发生炎症和氧化还原失调的机制。 结论:本文研究了急性心肌缺血再灌注所致的炎症反应和氧化还原紊乱,为靶向氧化还原失调提供了可能的治疗方案。,以减轻AMI后炎症反应的有害影响,从而减少心肌梗死的大小,预防心力衰竭。
关键词: 心肌缺血/再灌注损伤,氧化还原失调,炎症,活性氧,氧化应激,中性粒细胞。
Current Medicinal Chemistry
Title:The Role of Redox Dysregulation in the Inflammatory Response to Acute Myocardial Ischaemia-reperfusion Injury - Adding Fuel to the Fire
Volume: 25 Issue: 11
关键词: 心肌缺血/再灌注损伤,氧化还原失调,炎症,活性氧,氧化应激,中性粒细胞。
摘要: Background: The inflammatory response to acute myocardial ischaemia/ reperfusion injury (IRI) plays a critical role in determining myocardial infarct (MI) size, and subsequent post-MI left ventricular (LV) remodelling, making it a potential therapeutic target for improving clinical outcomes in patients presenting with an acute myocardial infarction (AMI). Recent experimental studies using advanced imaging and molecular techniques, have yielded new insights into the mechanisms through which reactive oxygen species (ROS) contribute to the inflammatory response induced by acute myocardial IRI - “adding fuel to the fire”. The infiltration of inflammatory cells into the MI zone, leads to elevated myocardial concentrations of ROS, cytokine release, and activation of apoptotic and necrotic death pathways. Anti-oxidant and anti-inflammatory therapies have failed to protect the heart against acute myocardial IRI. This may be, in part, due to a lack of understanding of the time course, nature and mechanisms of the inflammation and redox dysregulation, which occur in the setting of acute myocardial IRI.
Conclusion: In this article, we examine the inflammatory response and redox dysregulation induced by acute myocardial IRI, and highlight potential therapeutic options for targeting redox dysregulation, in order to attenuate the detrimental effects of the inflammatory response following an AMI, so as to reduce MI size and prevent heart failure.
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Cite this article as:
The Role of Redox Dysregulation in the Inflammatory Response to Acute Myocardial Ischaemia-reperfusion Injury - Adding Fuel to the Fire, Current Medicinal Chemistry 2018; 25 (11) . https://dx.doi.org/10.2174/0929867324666170329100619
DOI https://dx.doi.org/10.2174/0929867324666170329100619 |
Print ISSN 0929-8673 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-533X |
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