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心肌缺血和梗死中的细胞凋亡

Apoptosis in myocardial ischaemia and infarction.

作者信息

Krijnen P A J, Nijmeijer R, Meijer C J L M, Visser C A, Hack C E, Niessen H W M

机构信息

Department of Pathology, VU University Medical Centre, PO Box 7075, 1007MB Amsterdam, The Netherlands.

出版信息

J Clin Pathol. 2002 Nov;55(11):801-11. doi: 10.1136/jcp.55.11.801.

DOI:10.1136/jcp.55.11.801
PMID:12401816
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1769793/
Abstract

Recent studies indicate that, in addition to necrosis, apoptosis also plays a role in the process of tissue damage after myocardial infarction, which has pathological and therapeutic implications. This review article will discuss studies in which the role and mechanisms of apoptosis in myocardial infarction were analysed in vivo and in vitro in humans and in animals.

摘要

最近的研究表明，除坏死外，细胞凋亡在心肌梗死后的组织损伤过程中也起作用，这具有病理和治疗意义。这篇综述文章将讨论在体内和体外对人类和动物心肌梗死中细胞凋亡的作用和机制进行分析的研究。

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本文引用的文献

1
Apoptosis: a guide for the perplexed.细胞凋亡：解惑指南。
Trends Pharmacol Sci. 2002 Jan;23(1):19-24. doi: 10.1016/s0165-6147(00)01867-8.
2
In cardiomyocyte hypoxia, insulin-like growth factor-I-induced antiapoptotic signaling requires phosphatidylinositol-3-OH-kinase-dependent and mitogen-activated protein kinase-dependent activation of the transcription factor cAMP response element-binding protein.在心肌细胞缺氧过程中，胰岛素样生长因子-I诱导的抗凋亡信号传导需要磷脂酰肌醇-3-羟基激酶依赖性和丝裂原活化蛋白激酶依赖性激活转录因子环磷酸腺苷反应元件结合蛋白。
Circulation. 2001 Oct 23;104(17):2088-94. doi: 10.1161/hc4201.097133.
3
Annexin V staining during reperfusion detects cardiomyocytes with unique properties.再灌注期间的膜联蛋白V染色可检测出具有独特特性的心肌细胞。
Am J Physiol Heart Circ Physiol. 2001 Nov;281(5):H1931-7. doi: 10.1152/ajpheart.2001.281.5.H1931.
4
Hepatocyte growth factor protects cardiac myocytes against oxidative stress-induced apoptosis.肝细胞生长因子可保护心肌细胞免受氧化应激诱导的凋亡。
Free Radic Biol Med. 2001 Oct 1;31(7):902-10. doi: 10.1016/s0891-5849(01)00663-3.
5
Phosphorylation of proteins and apoptosis induced by c-Jun N-terminal kinase1 activation in rat cardiomyocytes by H(2)O(2) stimulation.H(2)O(2)刺激诱导大鼠心肌细胞中c-Jun氨基末端激酶1激活所引起的蛋白质磷酸化和细胞凋亡。
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6
Release of mitochondrial cytochrome c and activation of cytosolic caspases induced by myocardial ischaemia.心肌缺血诱导的线粒体细胞色素c释放及胞质半胱天冬酶激活
Biochim Biophys Acta. 2001 Sep 28;1537(2):101-9. doi: 10.1016/s0925-4439(01)00062-x.
7
Important role of energy-dependent mitochondrial pathways in cultured rat cardiac myocyte apoptosis.能量依赖的线粒体途径在培养的大鼠心肌细胞凋亡中的重要作用。
Am J Physiol Heart Circ Physiol. 2001 Oct;281(4):H1637-47. doi: 10.1152/ajpheart.2001.281.4.H1637.
8
Heart-targeted overexpression of caspase3 in mice increases infarct size and depresses cardiac function.小鼠心脏靶向性过表达半胱天冬酶3会增加梗死面积并降低心脏功能。
Proc Natl Acad Sci U S A. 2001 Aug 14;98(17):9977-82. doi: 10.1073/pnas.161120198. Epub 2001 Aug 7.
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Antioxid Redox Signal. 2001 Jun;3(3):403-13. doi: 10.1089/15230860152409059.
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JAK/STAT signaling is associated with cardiac dysfunction during ischemia and reperfusion.JAK/STAT信号传导与缺血再灌注期间的心脏功能障碍有关。
Circulation. 2001 Jul 17;104(3):325-9. doi: 10.1161/01.cir.104.3.325.