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参与心肌缺血再灌注损伤和心脏保护的新型分子靶点。

Novel Molecular Targets Participating in Myocardial Ischemia-Reperfusion Injury and Cardioprotection.

作者信息

Liu Nan-Bo, Wu Min, Chen Chen, Fujino Masayuki, Huang Jing-Song, Zhu Ping, Li Xiao-Kang

机构信息

Department of Cardiac Surgery, Guangdong Cardiovascular Institute, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, Guangdong 510100, China.

Division of Transplantation Immunology, National Research Institute for Child Health and Development, 2-10-1 Okura, Setagaya-ku, Tokyo 157-8535, Japan.

出版信息

Cardiol Res Pract. 2019 May 28;2019:6935147. doi: 10.1155/2019/6935147. eCollection 2019.

DOI:10.1155/2019/6935147
PMID:31275641
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6558612/
Abstract

Worldwide morbidity and mortality from acute myocardial infarction (AMI) and related heart failure remain high. While effective early reperfusion of the criminal coronary artery after a confirmed AMI is the typical treatment at present, collateral myocardial ischemia-reperfusion injury (MIRI) and pertinent cardioprotection are still challenging to address and have inadequately understood mechanisms. Therefore, unveiling the related novel molecular targets and networks participating in triggering and resisting the pathobiology of MIRI is a promising and valuable frontier. The present study specifically focuses on the recent MIRI advances that are supported by sophisticated bio-methodology in order to bring the poorly understood interrelationship among pro- and anti-MIRI participant molecules up to date, as well as to identify findings that may facilitate the further investigation of novel targets.

摘要

全球范围内,急性心肌梗死(AMI)及相关心力衰竭导致的发病率和死亡率仍然很高。虽然确诊AMI后对罪犯冠状动脉进行有效的早期再灌注是目前的典型治疗方法,但心肌缺血再灌注损伤(MIRI)及相关心脏保护仍是具有挑战性的问题,其机制尚未得到充分了解。因此,揭示参与引发和抵抗MIRI病理生物学过程的相关新分子靶点和网络是一个有前景且有价值的前沿领域。本研究特别关注近期在先进生物方法学支持下取得的MIRI研究进展,以便更新对促MIRI和抗MIRI参与分子之间鲜为人知的相互关系的认识,并确定可能有助于进一步研究新靶点的研究结果。

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本文引用的文献

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Multitarget Strategies to Reduce Myocardial Ischemia/Reperfusion Injury: JACC Review Topic of the Week.多靶点策略减少心肌缺血/再灌注损伤:美国心脏病学会评论专题的一周。
J Am Coll Cardiol. 2019 Jan 8;73(1):89-99. doi: 10.1016/j.jacc.2018.09.086.
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Analyses of changes in myocardial long non-coding RNA and mRNA profiles after severe hemorrhagic shock and resuscitation via RNA sequencing in a rat model.通过 RNA 测序分析大鼠严重失血性休克及复苏后心肌长非编码 RNA 和 mRNA 谱的变化。
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BRG1 regulates NOX gene transcription in endothelial cells and contributes to cardiac ischemia-reperfusion injury.
苏木酮A在炎症相关疾病中的研究进展
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Electroacupuncture posttreatment attenuates the inflammatory injury in rats after MIRI through PPARγ/NF-κb pathway.电针后处理通过PPARγ/NF-κb通路减轻大鼠心肌缺血再灌注损伤后的炎症损伤。
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Tilianin attenuates inflammasome activation in endothelial progenitor cells to mitigate myocardial ischemia-reperfusion injury.替利定通过减轻内皮祖细胞中的炎症小体激活来减轻心肌缺血再灌注损伤。
PLoS One. 2024 Oct 10;19(10):e0311624. doi: 10.1371/journal.pone.0311624. eCollection 2024.
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