|本期目录/Table of Contents|

[1]蔡志亮,蔡建航 综述,习瑾昆 审校.线粒体-锌离子-内质网与心肌缺血再灌注损伤[J].天津医科大学学报,2018,24(04):366-369.
点击复制

线粒体-锌离子-内质网与心肌缺血再灌注损伤(PDF)
分享到：

《天津医科大学学报》[ISSN:1006-8147/CN:12-1259/R]

卷:
24卷
期数:
2018年04期
页码:
366-369
栏目:
综述
出版日期:
2018-07-20

文章信息/Info

Title:
-
作者:
蔡志亮; 蔡建航 综述; 习瑾昆 审校
华北理工大学医学实验研究中心， 唐山 063000
Author(s):
-
关键词:
线粒体; 锌离子; 内质网; 心肌保护
Keywords:
-
分类号:
R363
DOI:
-
文献标志码:
Ａ
摘要:
在急性心肌梗死引发缺血再灌注损伤的研究中，线粒体、锌离子、内质网扮演着重要角色，并且三者在再灌注损伤中密切相关、相互作用。抑制内质网应激可能通过调节线粒体膜通透性转换孔的开放来发挥心肌线粒体保护作用，锌离子可能介导心肌保护的“内质网-线粒体对话”机制。但内质网应激感受器IRE1与锌离子、线粒体之间关联性的研究较少，阐明其在心肌缺血再灌注损伤中的作用及机制是亟待解决的问题。本文总结了早期研究的重要成果并对接下来的研究方向提出设想。
Abstract:
-

参考文献/References:


[1] 潘蓉蓉, 金永喜, 朱文宗. PI3K/Akt信号通路介导的细胞凋亡机制研究进展[J]. 浙江中西医结合杂志, 2013, (1): 70
[2] Ding G, Zhao J, Jiang D. Allicin inhibits oxidative stress-induced mitochondrial dysfunction and apoptosis by promoting PI3K/AKT and CREB/ERK signaling in osteoblast cells[J]. Exp Ther Med, 2016, 11(6): 2553
[3] Ovize M, Baxter G F, Di Lisa F, et al. Postconditioning and protection from reperfusion injury: where do we stand Position paper from the Working Group of Cellular Biology of the Heart of the European Society of Cardiology[J]. Cardiovasc Res, 2010, 87(3): 406
[4] Sunaga D, Tanno M, Kuno A, et al. Accelerated recovery of mitochondrial membrane potential by GSK-3beta inactivation affords cardiomyocytes protection from oxidant-induced necrosis[J]. PLoS One, 2014, 9(11): e112529
[5] 贺永贵, 李王芳, 伊红丽. 黄芪甲苷抑制GSK-3β活性介导大鼠心肌缺血/再灌注损伤作用的线粒体机制研究[J]. 中国药理学通报, 2014, (3): 402
[6] Xie Y, He Y, Cai Z, et al. Tauroursodeoxycholic acid inhibits endoplasmic reticulum stress, blocks mitochondrial permeability transition pore opening, and suppresses reperfusion injury through GSK-3ss in cardiac H9c2 cells[J]. Amer J of transl res, 2016, 8(11): 4586
[7] Cheng Y, Xia Z, Han Y, et al. Plant Natural Product Formononetin Protects Rat Cardiomyocyte H9c2 Cells against Oxygen Glucose Deprivation and Reoxygenation via Inhibiting ROS Formation and Promoting GSK-3beta Phosphorylation[J]. Oxid Med Cell Longev, 2016, (2016): 2060874
[8] Chanoit G, Zhou J, Lee S, et al. Inhibition of phosphodiesterases leads to prevention of the mitochondrial permeability transition pore opening and reperfusion injury in cardiac H9c2 cells[J]. Cardiovasc Drugs Ther, 2011, 25(4): 299
[9] Timmers L, Pasterkamp G, de Hoog V C, et al. The innate immune response in reperfused myocardium[J]. Cardiovasc Res, 2012, 94(2): 276
[10] Burwell L S, Nadtochiy S M, Brookes P S. Cardioprotection by metabolic shut-down and gradual wake-up[J]. J Mol Cell Cardiol, 2009, 46(6): 804
[11] Chouchani E T, Pell V R, Gaude E, et al. Ischaemic accumulation of succinate controls reperfusion injury through mitochondrial ROS[J]. Nature, 2014, 515(7527): 431
[12] Chouchani E T, Pell V R, James A M, et al. A Unifying Mechanism for Mitochondrial Superoxide Production during Ischemia-Reperfusion Injury[J]. Cell metabolism, 2016, 23(2): 254
[13] Lee S R, Noh S J, Pronto J R, et al. The Critical Roles of Zinc: Beyond Impact on Myocardial Signaling[J]. Korean J Physiol Pharmacol, 2015, 19(5): 389
[14] Chabosseau P, Tuncay E, Meur G, et al. Mitochondrial and ER-targeted eCALWY probes reveal high levels of free Zn2+[J]. ACS Chem Biol, 2014, 9(9): 2111
[15] Kiedrowski L. Proton-dependent zinc release from intracellular ligands[J]. J Neurochem, 2014, 130(1): 87
[16] Viswanath K, Bodiga S, Balogun V, et al. Cardioprotective effect of zinc requires ErbB2 and Akt during hypoxia/reoxygenation[J]. Biometals, 2011, 24(1): 171
[17] An W L, Pei J J, Nishimura T, et al. Zinc-induced anti-apoptotic effects in SH-SY5Y neuroblastoma cells via the extracellular signal-regulated kinase 1/2[J]. Brain Res Mol Brain Res, 2005, 135(1-2): 40
[18] Ilouz R, Kaidanovich O, Gurwitz D, et al. Inhibition of glycogen synthase kinase-3beta by bivalent zinc ions: insight into the insulin-mimetic action of zinc[J]. Biochem Biophys Res Commun, 2002, 295(1): 102
[19] Feyzizadeh S, Badalzadeh R. Application of ischemic postconditioning’s algorithms in tissues protection: response to methodological gaps in preclinical and clinical studies[J]. J Cell Mol Med, 2017, 21(10): 2257
[20] Huang J, Xu D, Guo Q, et al. Remote ischemic post-conditioning improves myocardial dysfunction via the risk and safe pathways in a rat model of severe hemorrhagic shock[J]. Shock, 2017
[21] Xu Z, Kim S, Huh J. Zinc plays a critical role in the cardioprotective effect of postconditioning by enhancing the activation of the RISK pathway in rat hearts[J]. J Mol Cell Cardiol, 2014, (66): 12
[22] Cohen P, Frame S. The renaissance of GSK3[J]. Nat Rev Mol Cell Biol, 2001, 2(10): 769
[23] Chanoit G, Lee S, Xi J, et al. Exogenous zinc protects cardiac cells from reperfusion injury by targeting mitochondrial permeability transition pore through inactivation of glycogen synthase kinase-3beta[J]. Am J Physiol Heart Circ Physiol, 2008, 295(3): 1227
[24] Xi J, Tian W, Zhang L, et al. Morphine prevents the mitochondrial permeability transition pore opening through NO/cGMP/PKG/Zn2+/GSK-3beta signal pathway in cardiomyocytes[J]. Am J Physiol Heart Circ Physiol, 2010, 298(2): 601
[25] 贺永贵, 张义东, 张国彬. 锌离子的心肌线粒体保护作用及其机制研究[J]. 中国药学杂志, 2016, (17): 1472
[26] 贺永贵, 张义东, 张国彬. 锌离子参与白藜芦醇的心肌线粒体保护作用及其机制研究[J]. 中国新药杂志, 2016, (8): 928
[27] Krezel A, Hao Q, Maret W. The zinc/thiolate redox biochemistry of metallothionein and the control of zinc ion fluctuations in cell signaling[J]. Arch Biochem Biophys, 2007, 463(2): 188
[28] Costello L C, Franklin R B. Cytotoxic/tumor suppressor role of zinc for the treatment of cancer: an enigma and an opportunity[J]. Expert Rev Anticancer Ther, 2012, 12(1): 121
[29] Minamino T, Kitakaze M. ER stress in cardiovascular disease[J]. J Mol Cell Cardiol, 2010, 48(6): 1105
[30] Gallo A, Vannier C, Galli T. Endoplasmic Reticulum-Plasma Membrane Associations:Structures and Functions[J]. Annu Rev Cell Dev Biol, 2016, (32): 279
[31] Hong J, Kim K, Kim J H. The Role of Endoplasmic Reticulum Stress in Cardiovascular Disease and Exercise[J]. 2017, ( 2017): 2049217
[32] Okumura N, Kitahara M, Okuda H, et al. Sustained Activation of the Unfolded Protein Response Induces Cell Death in Fuchs' Endothelial Corneal Dystrophy[J]. Invest Ophthalmol Vis Sci, 2017, 58(9): 3697
[33] Wu H, Tang Q, Yang J, et al. Atorvastatin ameliorates myocardial ischemia/reperfusion injury through attenuation of endoplasmic reticulum stress-induced apoptosis[J]. Int J Clin Exp Med, 2014, 7(12): 4915
[34] Bai S, Cheng L, Yang Y, et al. C1q/TNF-Related Protein 9 Protects Diabetic Rat Heart against Ischemia Reperfusion Injury: Role of Endoplasmic Reticulum Stress[J]. 2016, (2016): 1902025
[35] Miki T, Miura T, Hotta H, et al. Endoplasmic reticulum stress in diabetic hearts abolishes erythropoietin-induced myocardial protection by impairment of phospho-glycogen synthase kinase-3beta-mediated suppression of mitochondrial permeability transition[J]. Diabetes, 2009, 58(12): 2863
[36] Wang G, Huang H, Zheng H, et al. Zn2+ and mPTP mediate endoplasmic reticulum stress inhibition-induced cardioprotection against myocardial ischemia/reperfusion injury[J]. Biol Trace Elem Res, 2016, 174(1): 189
[37] Zhang Y, Xia Z, La Cour K H, et al. Activation of Akt rescues endoplasmic reticulum stress-impaired murine cardiac contractile function via glycogen synthase kinase-3beta-mediated suppression of mitochondrial permeation pore opening[J]. Antioxid Redox Signal, 2011, 15(9): 2407
[38] Yamasaki S, Hasegawa A, Hojyo S, et al. A novel role of the L-type calcium channel alpha1D subunit as a gatekeeper for intracellular zinc signaling: zinc wave[J]. PLoS One, 2012, 7(6): 39654
[39] Homma K, Ichijo H. Zinc depletion and ER stress[J]. Nihon Rinsho, 2016, 74(7): 1228
[40] Homma K, Fujisawa T, Tsuburaya N, et al. SOD1 as a molecular switch for initiating the homeostatic ER stress response under zinc deficiency[J]. Mol Cell, 2013, 52(1): 75
[41] Xu Z, Zhou J. Zinc and myocardial ischemia/reperfusion injury[J]. Biometals, 2013, 26(6): 863
[42] 李王芳. 锌离子在内质网应激抑制剂诱导心肌保护中的作用[D]. 河北联合大学, 2014
[43] Naughton M C, McMahon J M, FitzGerald U. Differential activation of ER stress pathways in myelinating cerebellar tracts[J]. Int J Dev Neurosci, 2015, 47(Pt B): 347
[44] Wong M Y, DiChiara A S, Suen P H, et al. Adapting Secretory Proteostasis and Function Through the Unfolded Protein Response[J]. Curr Top Microbiol Immunol, 2017, [Epub ahead of print]
[45] 郑志刚. IRE1分子通路在内质网预应激条件下对肝细胞缺氧损伤的保护机制[D]. 第四军医大学, 2012
[46] Gardner B M, Walter P. Unfolded proteins are Ire1-activating ligands that directly induce the unfolded protein response[J]. Science, 2011, 333(6051): 1891 [47] Rozpedek W, Nowak A, Pytel D, et al. Molecular basis of human diseases and targeted therapy based on small-molecule inhibitors of ER stress-induced signaling pathways[J]. Curr Mol Med, 2017, 17(2): 118 [48] Nguyen T S L, Kohno K, Kimata Y. Zinc depletion activates the endoplasmic reticulum-Stress Sensor ire1via pleiotropic mechanisms[J]. Biosci Biotechnol Biochem, 2014, 77(6): 1337

相似文献/References:

[1]孙亚军,傅正,朱志峰,等.基因芯片分析三肽化合物酪丝亮肽对人肝癌基因表达谱的影响[J].天津医科大学学报,2013,19(05):353.
[2]王艳辉,金玉 综述,任丽 审校.线粒体SIRT3在肿瘤发生和治疗中作用的研究进展[J].天津医科大学学报,2021,27(05):541.
[3]张英,李豫峰,王婷,等.不同时期胚胎线粒体拷贝数与胚胎自身形态学分型的关系研究[J].天津医科大学学报,2023,29(01):55.
　ZHANG Ying,LI Yu-feng,WANG Ting,et al.Study on the relationship between the mitochondrial copy number of embryos at different stages and the morphological types of embryos[J].Journal of Tianjin Medical University,2023,29(04):55.
[4]柴鹏程,韩海波,胡振杰,等.左西孟旦对脓毒症心肌损伤小鼠的保护作用及机制研究[J].天津医科大学学报,2023,29(05):481.
　CHAI Peng-cheng,HAN Hai-bo,HU Zhen-jie,et al.Protective effect and mechanism of Levosimendan on sepsis induced myocardial injury in mice[J].Journal of Tianjin Medical University,2023,29(04):481.
[5]刘思琪,郝名英,黄欣宇,等.端粒酶TERT通过向线粒体转位抵抗胃癌细胞铁死亡的发生机制[J].天津医科大学学报,2024,30(02):110.[doi:10.20135/j.issn.1006-8147.2024.02.0110]
　LIU Siqi,HAO Mingying,HUANG Xinyu,et al.The mechanism of telomerase TERT resisting ferroptosis in gastric cancer cells by translocating to mitochondria[J].Journal of Tianjin Medical University,2024,30(04):110.[doi:10.20135/j.issn.1006-8147.2024.02.0110]

备注/Memo

备注/Memo:
-
更新日期/Last Update: 2018-07-20