切换至 "中华医学电子期刊资源库"

中华损伤与修复杂志(电子版) ›› 2015, Vol. 10 ›› Issue (02) : 175 -179. doi: 10.3877/cma.j.issn.1673-9450.2015.02.014

所属专题: 文献

综述

脓毒症心肌线粒体改变与干预的研究进展
何鑫1, 张勤1,()   
  1. 1. 200025 上海交通大学医学院附属瑞金医院灼伤整形外科
  • 收稿日期:2015-02-21 出版日期:2015-04-01
  • 通信作者: 张勤

Research progress in the changes and management of myocardial mitochondria during sepsis

Xin He1, Qin Zhang1,()   

  1. 1. Department of Burn and Plastic Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China
  • Received:2015-02-21 Published:2015-04-01
  • Corresponding author: Qin Zhang
  • About author:
    Corresponding author: Zhang Qin, Email:
引用本文:

何鑫, 张勤. 脓毒症心肌线粒体改变与干预的研究进展[J/OL]. 中华损伤与修复杂志(电子版), 2015, 10(02): 175-179.

Xin He, Qin Zhang. Research progress in the changes and management of myocardial mitochondria during sepsis[J/OL]. Chinese Journal of Injury Repair and Wound Healing(Electronic Edition), 2015, 10(02): 175-179.

约50%的脓毒症患者合并心脏收缩功能降低和心输出量减少,约11.4%患者甚至出现心功能衰竭。目前认为,脓毒症时心肌线粒体形态和功能的改变是心肌收缩功能降低的重要原因。长期以来人们对脓毒症时的心肌线粒体改变与干预的基础和临床研究开展了大量的实验。本文就近年来国内外有关脓毒症时心肌线粒体结构、功能、自噬作用、凋亡作用的改变与干预方面的研究进展做了总结论述。

Reduction of cardiac output and systolic function occurs in almost 50% septic patients .Meanwhile, 11.4% of them develop heart failure.Recently, it is believed that structural and functional changes of myocardial mitochondria are the main causes of cardiac systolic function's reduction during sepsis. There have been a lot of the basic and clinical studies on septic changes and management of myocardial mitochondria for a long time. This review tries to summarize the domestic and foreign research progresses in the changes and management concerning the structure and function of myocardial mitochondria, mitophagy as well as apoptosis during sepsis.

1
Zhou J, Qian C, Zhao M, et al. Epidemiology and outcome of severe sepsis and septic shock in intensive care units in mainland china[J]. PLoS One, 2014, 9(9): e107181.
2
Harrois A, Huet O, Duranteau J, et al. Alterations of mitochondrial function in sepsis and critical illness[J]. Curr Opin Anaesthesiol, 2009, 22(2): 143-149.
3
Gotloib L, Shostak A, Galdi P, et al. Loss of microvascular negative charges accompanied by interstitial edema in septic rats′ heart[J]. Circ Shock, 1992, 36(1): 45-56.
4
Suliman HB, Welty-Wolf KE, Carraway M, et al. Lipopolysaccharide induces oxidative cardiac mitochondrial damage and biogenesis[J]. Cardiovasc Res, 2004, 64(2): 279-288.
5
Soriano FG, Nogueira AC, Caldini EG, et al. Potential role of poly(adenosine 5′-diphosphate-ribose) polymerase activation in the pathogenesis of myocardial contractile dysfunction associated with human septic shock[J]. Crit Care Med, 2006, 34(4): 1073-1079.
6
Ahmed LA. Protective effects of magnesium supplementation on metabolic energy derangements in lipopolysaccharide-induced cardiotoxicity in mice[J]. Eur J Pharmacol, 2012, 694(1-3): 75-81.
7
Smeding L, Leong-Poi H, Hu P, et al. Salutary effect of resveratrol on sepsis-induced myocardial depression[J]. Crit Care Med, 2012, 40(6): 1896-1907.
8
Smeding L, Plötz FB, Groeneveld AB, et al. Structural changes of the heart during severe sepsis or septic shock[J]. Shock, 2012, 37(5): 449-456.
9
Vanasco V, Saez T, Magnani ND, et al. Cardiac mitochondrial biogenesis in endotoxemia is not accompanied by mitochondrial function recovery[J]. Free Radic Biol Med, 2014, 77: 1-9.
10
Vanasco V, Magnani ND, Cimolai MC, et al. Endotoxemia impairs heart mitochondrial function by decreasing electron transfer, ATP synthesis and ATP content without affecting membrane potential[J]. J Bioenerg Biomembr, 2012, 44(2): 243-252.
11
Correa TD, Vuda M, Blaser AR, et al. Effect of treatment delay on disease severity and need for resuscitation in porcine fecal peritonitis[J]. Crit Care Med, 2012, 40(10): 2841-2849.
12
Regueira T, Djafarzadeh S, Brandt S, et al. Oxygen transport and mitochondrial function in porcine septic shock, cardiogenic shock, and hypoxaemia[J]. Acta Anaesthesiol Scand, 2012, 56(7): 846-859.
13
Duarte S, Arango D, Parihar A, et al. Apigenin protects endothelial cells from lipopolysaccharide (LPS)-induced inflammation by decreasing caspase-3 activation and modulating mitochondrial function[J]. Int J Mol Sci, 2013, 14(9): 17664-17679.
14
Groening P, Huang Z, La Gamma EF, et al. Glutamine restores myocardial cytochrome C oxidase activity and improves cardiac function during experimental sepsis[J]. JPEN J Parenter Enteral Nutr, 2011, 35(2): 249-254.
15
Verma R, Huang Z, Deutschman CS, et al. Caffeine restores myocardial cytochrome oxidase activity and improves cardiac function during sepsis[J]. Crit Care Med, 2009, 37(4): 1397-1402.
16
Rocha M, Herance R, Rovira S, et al. Mitochondrial dysfunction and antioxidant therapy in sepsis[J]. Infect Disord Drug Targets, 2012, 12(2): 161-178.
17
Supinski GS, Murphy MP, Callahan LA. MitoQ administration prevents endotoxin-induced cardiac dysfunction[J]. Am J Physiol Regul Integr Comp Physiol, 2009, 297(4): 1095-1102.
18
Zang QS, Sadek H, Maass DL, et al. Specific inhibition of mitochondrial oxidative stress suppresses inflammation and improves cardiac function in a rat pneumonia-related sepsis model[J]. Am J Physiol Heart Circ Physiol, 2012, 302(9): H1847-H1859.
19
Torraco A, Carrozzo R, Piemonte F, et al. Effects of levosimendan on mitochondrial function in patients with septic shock: a randomized trial[J]. Biochimie, 2014, 102: 166-173.
20
Hao E, Lang F, Chen Y, et al. Resveratrol alleviates endotoxin-induced myocardial toxicity via the Nrf2 transcription factor[J]. PLoS One, 2013, 8(7): e69452.
21
Pan S, Wang N, Bisetto S, et al. Downregulation of adenine nucleotide translocator 1 exacerbates tumor necrosis factor-α mediated cardiac inflammatory responses[J]. Am J Physiol Heart Circ Physiol, 2015, 308(1): H39-H48.
22
Zhu H, Shan L, Schiller PW, et al. Histone deacetylase-3 activation promotes tumor necrosis factor-alpha (TNF-alpha) expression in cardiomyocytes during lipopolysaccharide stimulation[J]. J Biol Chem, 2010, 285(13): 9429-9436.
23
López A, Lorente JA, Steingrub J, et al. Multiple-center, randomized, placebo-controlled, double-blind study of the nitric oxide synthase inhibitor 546C88: effect on survival in patients with septic shock[J]. Crit Care Med, 2004, 32(1): 21-30.
24
Escames G, López LC, Ortiz F, et al. Attenuation of cardiac mitochondrial dysfunction by melatonin in septic mice[J]. FEBS J, 2007, 274(8): 2135-2147.
25
Ortiz F, García JA, Acuña-Castroviejo D, et al. The beneficial effects of melatonin against heart mitochondrial impairment during sepsis: inhibition of iNOS and preservation of nNOS[J]. J Pineal Res, 2014, 56(1): 71-81.
26
Xu C, Yi C, Wang H, et al. Mitochondrial nitric oxide synthase participates in septic shock myocardial depression by nitric oxide overproduction and mitochondrial permeability transition pore opening[J]. Shock, 2012, 37(1): 110-115.
27
Valerio A, Nisoli E. Nitric oxide, interorganelle communication, and energy flow: a novel route to slow aging[J]. Front Cell Dev Biol, 2015, 3(6): 1-11.
28
Bangash MN, Kong ML, Pearse RM. Use of inotropes and vasopressor agents in critically ill patients[J]. Br J Pharmacol, 2012, 165(7): 2015-2033.
29
Vajapey R, Rini D, Walston J. The impact of age-related dysregulation of the angiotensin system on mitochondrial redox balance[J]. Front Physiol, 2014, 24(5): 439.
30
Yang CS, Yuk JM, Kim JJ, et al. Small heterodimer partner-targeting therapy inhibits systemic inflammatory responses through mitochondrial uncoupling protein 2[J]. PLoS One, 2013, 8(5): e63435.
31
Righi V, Constantinou C, Mintzopoulos D, et al. Mitochondria-targeted antioxidant promotes recovery of skeletal muscle mitochondrial function after burn trauma assessed by in vivo 31P nuclear magnetic resonance and electron paramagnetic resonance spectroscopy[J]. FASEB J, 2013, 27(6): 2521-2530.
32
Zang QS, Martinez B, Yao X, et al. Sepsis-induced cardiac mitochondrial dysfunction involves altered mitochondrial-localization of tyrosine kinase Src and tyrosine phosphatase SHP2[J]. PLoS One, 2012, 7(8): e43424.
33
Drosatos K, Khan RS, Trent CM, et al. Peroxisome proliferator-activated receptor-γ activation prevents sepsis-related cardiac dysfunction and mortality in mice[J]. Circ Heart Fail, 2013, 6(3): 550-562.
34
Piquereau J, Godin R, Deschênes S, et al. Protective role of PARK2/Parkin in sepsis-induced cardiac contractile and mitochondrial dysfunction[J]. Autophagy, 2013, 9(11): 1837-1851.
35
Hsieh CH, Pai PY, Hsueh HW, et al. Complete induction of autophagy is essential for cardioprotection in sepsis[J]. Annals of surgery, 2011, 253(6): 1190-1200.
36
Yuan H, Perry CN, Huang C, et al. LPS-induced autophagy is mediated by oxidative signaling in cardiomyocytes and is associated with cytoprotection[J]. Am J Physiol Heart Circ Physiol, 2009, 296(2): H470-H479.
37
Turdi S, Han X, Huff AF, et al. Cardiac-specific overexpression of catalase attenuates lipopolysaccharide-induced myocardial contractile dysfunction: role of autophagy[J]. Free Radic Biol Med, 2012, 53(6): 1327-1338.
38
Unuma K, Aki T, Funakoshi T, et al. Cobalt protoporphyrin accelerates TFEB activation and lysosome reformation during LPS-induced septic insults in the rat heart[J]. PLoS One, 2013, 8(2): e56526.
39
Li L, Hu BC, Chen CQ, et al. Role of mitochondrial damage during cardiac apoptosis in septic rats[J]. Chin Med J (Engl), 2013, 126(10): 1860-1866.
40
Takasu O, Gaut JP, Watanabe E, et al. Mechanisms of cardiac and renal dysfunction in patients dying of sepsis[J]. Am J Respir Crit Care Med, 2013, 187(5): 509-517.
41
Yang Z, Liu Y, Deng W, et al. Hesperetin attenuates mitochondria-dependent apoptosis in lipopolysaccharide-induced H9C2 cardiomyocytes[J]. Mol Med Rep, 2014, 9(5): 1941-1946.
42
Tsai KL, Liang HJ, Yang ZD, et al. Early inactivation of PKCε associates with late mitochondrial translocation of Bad and apoptosis in ventricle of septic rat[J]. J Surg Res, 2014, 186(1): 278-286.
43
Tien YC, Lin JY, Lai CH, et al. Carthamus tinctorius L. prevents LPS-induced TNFalpha signaling activation and cell apoptosis through JNK1/2-NFkappaB pathway inhibition in H9c2 cardiomyoblast cells[J]. J Ethnopharmacol, 2010, 130(3): 505-513.
[1] 陈芬, 葛贝贝, 王小贤, 李明霞, 徐芳, 史坚, 郭冠军, 方爱娟, 史中青, 戚占如, 陈慧, 姚静. 左束支传导阻滞性心肌病心脏电-机械重构的实验研究[J/OL]. 中华医学超声杂志(电子版), 2024, 21(10): 978-985.
[2] 夏靖涵, 林凤娇, 王胰, 丁戈琦, 张清凤, 张红梅, 谢盛华, 李明星, 尹立雪, 李文华. 二尖瓣空间变化联合左心房应变对肥厚型心肌病合并左心室流出道梗阻的预测价值[J/OL]. 中华医学超声杂志(电子版), 2024, 21(06): 585-592.
[3] 王岚, 徐斌胜, 谢乐. 肥厚型心肌病的经胸超声心动图诊断与心电图表现特征[J/OL]. 中华医学超声杂志(电子版), 2024, 21(06): 593-596.
[4] 江雅婷, 刘林峰, 沈辰曦, 陈奔, 刘婷, 龚裕强. 组织相关巨噬素3 保护肺血管内皮糖萼治疗急性呼吸窘迫综合征的机制研究[J/OL]. 中华危重症医学杂志(电子版), 2024, 17(05): 353-362.
[5] 庄燕, 戴林峰, 张海东, 陈秋华, 聂清芳. 脓毒症患者早期生存影响因素及Cox 风险预测模型构建[J/OL]. 中华危重症医学杂志(电子版), 2024, 17(05): 372-378.
[6] 钟雅雯, 王煜, 王海臻, 黄莉萍. 肌苷通过抑制线粒体通透性转换孔开放缓解缺氧/复氧诱导的人绒毛膜滋养层细胞凋亡[J/OL]. 中华妇幼临床医学杂志(电子版), 2024, 20(05): 525-533.
[7] 黄程鑫, 陈莉, 刘伊楚, 王水良, 赖晓凤. OPA1 在乳腺癌组织的表达特征及在ER阳性乳腺癌细胞中的生物学功能研究[J/OL]. 中华细胞与干细胞杂志(电子版), 2024, 14(05): 275-284.
[8] 成人脓毒症患者β-内酰胺类抗生素延长输注专家共识编写组. 成人脓毒症患者β-内酰胺类抗生素延长输注专家共识[J/OL]. 中华重症医学电子杂志, 2024, 10(04): 313-324.
[9] 陈曦, 吴宗盛, 郑明珠, 邱海波. 胸腺萎缩在脓毒症免疫紊乱中的研究进展[J/OL]. 中华重症医学电子杂志, 2024, 10(04): 379-383.
[10] 杨翔, 郭兰骐, 谢剑锋, 邱海波. 转录组学在脓毒症诊疗中的临床研究进展[J/OL]. 中华重症医学电子杂志, 2024, 10(04): 384-388.
[11] 崔健, 夏青, 林云, 李光玲, 李心娜, 王位. 血小板与淋巴细胞比值、免疫球蛋白、心肌酶谱及心电图对中老年肝硬化患者病情及预后的影响[J/OL]. 中华消化病与影像杂志(电子版), 2024, 14(05): 400-406.
[12] 陈惠英, 邱敏珊, 邵汉权. 脓毒症诱发肠黏膜屏障功能损伤的风险因素模型构建与应用效果[J/OL]. 中华消化病与影像杂志(电子版), 2024, 14(05): 448-452.
[13] 贾玲玲, 滕飞, 常键, 黄福, 刘剑萍. 心肺康复在各种疾病中应用的研究进展[J/OL]. 中华临床医师杂志(电子版), 2024, 18(09): 859-862.
[14] 傅新露, 李之岳, 卢丹. 妊娠合并结肠癌穿孔致脓毒症休克一例并文献复习[J/OL]. 中华产科急救电子杂志, 2024, 13(04): 227-231.
[15] 郑屹, 刘莹, 张煜坤, 李广平, 陈康寅, 刘彤. 既往及新发心房颤动对急性心肌梗死患者远期卒中风险的影响[J/OL]. 中华脑血管病杂志(电子版), 2024, 18(05): 406-417.
阅读次数
全文


摘要


AI


AI小编
你好!我是《中华医学电子期刊资源库》AI小编,有什么可以帮您的吗?