心肌缺血-再灌注损伤的相关分子机制及防治

被引：14

作者：

李朝杰

龙明智

机构：

[1] 南京医科大学第二附属医院心内科

来源：

国际心血管病杂志 | 2011年 / 38卷 / 05期

关键词：

心肌; 缺血-再灌注损伤; 线粒体通透性转换孔; 钙超载;

D O I：

暂无

中图分类号：

R542.22 [];

学科分类号：

摘要：

心肌缺血-再灌注损伤是近年来心血管疾病领域研究的热点问题,现今对其损伤机制主要有以下认识:线粒体内膜通透性转换孔的开放诱导了细胞的凋亡,但是否线粒体内膜通透性转换孔是细胞凋亡最终效应器仍在争议中;钙离子超载可以作用于钙敏感受体和钙调蛋白激酶Ⅱ两个重要的钙离子生理靶点介导细胞的凋亡;大量活性氧释放介导氧爆发;内质网应激通路是不同于传统凋亡途径的新路径;中性粒细胞及炎症介质的浸润。而对其防治措施的研究主要包括:缺血预处理和后处理,药物治疗,干细胞移植。至今对心肌缺血-再灌注损伤分子机制及防治措施尚无明确统一的认定,此综述从分子水平讨论缺血-再灌注损伤的机制和防治。

引用

页码：273 / 276

页数：4

共 13 条

[1]

Reactive Oxygen Species–Activated Ca/Calmodulin Kinase IIδ Is Required for Late INa Augmentation Leading to Cellular Na and Ca Overload.[J].Stefan Wagner;Hanna M. Ruff;Sarah L. Weber;Sarah Bellmann;Thomas Sowa;Timo Schulte;Mark E. Anderson;Eleonora Grandi;Donald M. Bers;Johannes Backs;Luiz Belardinelli;Lars S. Maier.Circulation Research.2011, 5

[2]

Ischaemic pre-conditioning means an increased adenosine metabolism with decreased glycolytic flow in ischaemic pig myocardium [J].

Aberg, A. M. ;

Ahlstrom, K. ;

Abrahamsson, P. ;

Waldenstrom, A. ;

Ronquist, G. ;

Hauck, P. ;

Johansson, G. ;

Biber, B. ;

Haney, M. .

ACTA ANAESTHESIOLOGICA SCANDINAVICA, 2010, 54 (10) :1257-1264

[3]

Ischemic post-conditioning reduces infarct size of the in vivo rat heart: role of PI3-K, mTOR, GSK-3β, and apoptosis [J].

Claudia Wagner ;

Diana Tillack ;

Gregor Simonis ;

Ruth H. Strasser ;

Christof Weinbrenner .

Molecular and Cellular Biochemistry, 2010, 339 :135-147

[4]

Prolyl hydroxylase inhibition attenuates post-ischemic cardiac injury via induction of endoplasmic reticulum stress genes.[J].Ramesh Natarajan;Fadi N. Salloum;Bernard J. Fisher;Lisa Smithson;Jorge Almenara;Alpha A. Fowler.Vascular Pharmacology.2009, 2

[5]

Caspases and Kinases in a Death Grip [J].

Kurokawa, Manabu ;

Kornbluth, Sally .

CELL, 2009, 138 (05) :838-854

[6]

Role of reactive oxygen species (ROS) in angiotensin II-induced stimulation of the cardiac Na+/HCO3- cotransport [J].

De Giusti, Veronica C. ;

Garciarena, Carolina D. ;

Aiello, Ernesto A. .

JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 2009, 47 (05) :716-722

[7]

MitoKATP activity in healthy and ischemic hearts [J].

Costa, Alexandre D. T. ;

Garlid, Keith D. .

JOURNAL OF BIOENERGETICS AND BIOMEMBRANES, 2009, 41 (02) :123-126

[8]

Acidosis, oxygen, and interference with mitochondrial permeability transition pore formation in the early minutes of reperfusion are critical to postconditioning's success [J].

Cohen, Michael V. ;

Yang, Xi-Ming ;

Downey, James M. .

BASIC RESEARCH IN CARDIOLOGY, 2008, 103 (05) :464-471

[9]

Acute Coronary Care in the Elderly; Part II: ST-Segment–Elevation Myocardial Infarction: A Scientific Statement for Healthcare Professionals From the American Heart Association Council on Clinical Cardiology.[J].Karen P. Alexander;L Kristin Newby;Paul W. Armstrong;Christopher P. Cannon;W Brian Gibler;Michael W. Rich;Frans Van de Werf;Harvey D. White;W Douglas Weaver;Mary D. Naylor;Joel M. Gore;Harlan M. Krumholz;E Magnus Ohman.Circulation.2007, 19

[10]

Endoplasmic reticulum stress gene induction and protection from ischemia/reperfusion injury in the hearts of transgenic mice with a tamoxifen-regulated form of ATF6 [J].

Martindale, Joshua J. ;

Fernandez, Rayne ;

Thuerauf, Donna ;

Whittaker, Ross ;

Gude, Natalie ;

Sussman, Mark A. ;

Glembotski, Christopher C. .

CIRCULATION RESEARCH, 2006, 98 (09) :1186-1193

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