索引超出了数组界限。 文章摘要
|本期目录/Table of Contents|

[1]吕磊,王永园,徐军.线粒体活性氧在心肌缺血再灌注中的作用[J].国际心血管病杂志,2017,06:338-340,347.
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线粒体活性氧在心肌缺血再灌注中的作用(PDF)

《国际心血管病杂志》[ISSN:1006-6977/CN:61-1281/TN]

期数:
2017年06期
页码:
338-340,347
栏目:
综述
出版日期:
2017-11-25

文章信息/Info

Title:
-
作者:
吕磊王永园徐军
210002 南京军区南京总医院心脏内科干部病区
Author(s):
-
关键词:
活性氧 线粒体 缺血再灌注损伤 线粒体电子传递链
Keywords:
-
分类号:
-
DOI:
10.3969/j.issn.1673-6583.2017.06.005
文献标识码:
A
摘要:
活性氧(ROS)的过度生成是心肌缺血再灌注损伤的主要机制之一。线粒体是ROS的主要来源,也是再灌注心肌保护策略的关键靶点。再灌注早期产生的大量ROS可损伤心肌,但少量的ROS对心脏保护的氧化还原信号至关重要。该文介绍了线粒体ROS在心肌缺血再灌注损伤和保护中的作用。
Abstract:
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参考文献/References

[1] Angelova PR, Abramov AY. Functional role of mitochondrial reactive oxygen species in physiology[J]. Free Radic Biol Med, 2016, 100(11):81-85.
[2] Bartz RR, Suliman HB, Piantadosi CA. Redox mechanisms of cardiomyocyte mitochondrial protection[J]. Front Physiol, 2015, 6(10):291-298.
[3] Chen YR, Zweier JL. Cardiac mitochondria and reactive oxygen species generation[J]. Circ Res, 2014, 114(3):524-537.
[4] Korge P, John SA, Calmettes G, et al. Reactive oxygen species production induced by pore opening in cardiac mitochondria: The role of complex Ⅱ[J]. J Biol Chem, 2017, 292(24):9896-9905.
[5] Srinivasan S, Spear J, Chandran K, et al. Oxidative stress induced mitochondrial protein kinase A mediates cytochrome C oxidase dysfunction[J]. PLoS One, 2013, 8(10):e77129-e77144.
[6] Duicu OM, Lighezan R, Sturza A, et al. Assessment of mitochondrial dysfunction and monoamine oxidase contribution to oxidative stress in human diabetic hearts[J]. Oxid Med Cell Longev, 2016, 2016:8470394.
[7] Inagaki T, Akiyama T, Du CK, et al. Monoamine oxidase-induced hydroxyl radical production and cardiomyocyte injury during myocardial ischemia-reperfusion in rats[J]. Free Radic Res, 2016, 50(6):645-653.
[8] Faria A, Persaud SJ. Cardiac oxidative stress in diabetes: Mechanisms and therapeutic potential[J]. Pharmacol Ther, 2016, 172(12):50-62.
[9] Hernández-Reséndiz S, Chinda K, Ong S-B, et al. The role of redox dysregulation in the inflammatory response to acute myocardial ischaemia-reperfusion injury - adding fuel to the fire[J]. Curr Med Chem, 2017,24(42): 28356034-28356044.
[10] Yao X, Carlson D, Sun Y, et al. Mitochondrial ROS induces cardiac inflammation via a pathway through mtDNA damage in a pneumonia-related sepsis model[J]. PLoS One, 2015, 10(10):e0139416-e0139444.
[11] Murphy MP. Understanding and preventing mitochondrial oxidative damage[J]. Biochem Soc Trans, 2016, 44(5): 1219-1226.
[12] Kalogeris T, Bao Y, Korthuis RJ. Mitochondrial reactive oxygen species: a double edged sword in ischemia/reperfusion vs preconditioning[J]. Redox Biol, 2014, 2(1):702-714.
[13] Cohen MV, Downey JM. Signalling pathways and mechanisms of protection in pre- and postconditioning: historical perspective and lessons for the future[J]. Br J Pharmacol, 2015, 172(8):1913-1932.
[14] Galagudza MM, Sonin DL, Vlasov TD, et al. Remote vs. local ischaemic preconditioning in the rat heart: infarct limitation, suppression of ischaemic arrhythmia and the role of reactive oxygen species[J]. Int J Exp Pathol, 2016, 97(1):66-74.
[15] Andrienko T, Pasdois P, Rossbach A, et al. Real-time fluorescence measurements of ROS and [Ca2+] in ischemic/reperfused rat hearts:detectable increases occur only after mitochon--drial pore opening and are attenuated by ischemic preconditioning[J]. PLoS One, 2016, 11(12): 27907091-27907122.
[16] Dǎnilǎ MD, Privistirescu AI, Mirica SN, et al. Acute inhibition of monoamine oxidase and ischemic preconditioning in isolated rat hearts: interference with postischemic functional recovery but no effect on infarct size reduction[J]. Can J Physiol Pharmacol, 2015, 93(9):819-825.
[17] Madungwe NB, Zilberstein NF, Feng Y, et al. Critical role of mitochondrial ROS is dependent on their site of production on the electron transport chain in ischemic heart[J]. Am J Cardiovasc Dis, 2016, 6(3):93-108.
[18] Lonborg JT. Targeting reperfusion injury in the era of primary percutaneous coronary intervention: hope or hype?[J]. Heart, 2015, 101(20):1612-1618.

备注/Memo

备注/Memo:
基金项目:南京军区南京总医院科研基金(2014061)
通信作者:徐军,Email:xxujun305@sina.com
更新日期/Last Update: 2017-12-10