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|本期目录/Table of Contents|

自噬与病毒性心肌炎关系研究进展

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2016年第2期
页码:
221-225
栏目:
综述
出版日期:
2015-11-25

文章信息/Info

Title:
Research progress of relationship between autophagy and viral myocarditis
作者:
于建才赫嘉惠仲娇月赵德超
(哈尔滨医科大学附属第一医院心内科,黑龙江 哈尔滨 150001)
Author(s):
YU Jian-cai HE Jia-hui ZHONG Jiao-yue ZHAO De-chao
(Department of Cardiology, First Affiliated Hospital, Harbin Medical University, Harbin 150001, Heilongjiang, China)
关键词:
自噬病毒性心肌炎氧化应激病毒感染
Keywords:
autophagy viral myocarditis oxidative stress coronavirus infections
分类号:
R452.2
DOI:
-
文献标识码:
A
摘要:
自噬(autophagy)是细胞依赖溶酶体对胞内蛋白质和受损细胞器进行降解的一条重要途径。细胞自噬受各种因子的精密调节,是细胞清除损伤物质和维持细胞稳态的重要调节方式,与心血管疾病、肿瘤和神经退行性疾病发生密切相关[1]。近几年有文献报道病毒性心肌炎中存在细胞自噬现象[2~4],结合作者前期试验在小鼠病毒性心肌炎模型中亦观察到细胞自噬现象,因此本文就自噬与病毒性心肌炎的关系进行综述。
Abstract:
Autophagy is an important biological process in which the cytoplasmic constituents of protein and impaired organelles are sequestered in a double-membrane autophagosome and then delivered to the lysosome for degradation. Selective degradation of autophagy is highly regulated by various molecules. Autophagy is an important regulatory approach of clearing damaged cellular materials and maintaining cell homeostasis and is closely related to cardiovascular disease, tumors and neurodegenerative diseases. In recent years, there has been reported a phenomenon of autophagy in viral myocarditis. In our preliminary experiments of the mouse model of viral myocarditis, we also observed the phenomenon of autophagy. This review summarizes the research progress of the relationship between autophagy and viral myocarditis.

参考文献/References

[1]Essick EE,Sam F.Oxidative stress and autophagy in cardiac disease,neurological disorders, aging and cancer[J].Oxid Med Cell Longev,2010,3(3):168-177.
[2]Robinson SM,Tsueng G,Sin J.Coxsackievirus B exits the host cell in shed microvesicles displaying autophagosomal markers[J].PloS Pathoq,2014,10(4):e1004045.
[3]Koenig A,Sateriale A,Budd RC,et al.The role of sex differences in autophagy in the heart during coxsackievirus B3-induced myocarditis[J].Cardiovasc Transl Res,2014,7(2):182-191.
[4]Reddy J,Massilamany C,Buskiewicz I,et al.Autoimmunity in viral myocarditis[J].Curr Opin Rheumatol,2013,25(4):502-508.
[5]He C,Klionsky DJ.Regulation mechanisms and signaling pathways of autophagy[J].Annu Rev Genet,2009,43:67-93.
[6]Dadakhujaev S,Jung EJ,Noh HS,et al.Interplay between autophagy and apoptosis in TrkA-induced cell death[J].Autophagy,2009,5(1):103-105.
[7]Taylor R,Goldman SJ.Mitophagy and disease:new avenues for pharmacological intervention[J].Curr Pharm Des,2011,17(20):2056-2073.
[8]Gurusamy N,Das DK.Is autophagy a double-edged sword for the heart?[J].Acta Physiol Hung,2009,96(3):267-276.
[9]Dutta D,Calvani R,Bernabei R,et al.Contribution of impaired mitochondrial autophagy to cardiac aging: mechanisms and therapeutic opportunities[J].Circ Res,2012,110(8):1125-1138.
[10]Oka T,Hikoso S,Yamaguchi O,et al.Mitochondrial DNA that escapes from autophagy causes inflammation and heart failure[J].Nature,2012,485 (7397):251-255.
[11]Joubert PE,Meiffren G,Gregoire IP,et al.Autophagy induction by the pathogen receptor[J].Cell Host Microbe, 2009,6(4):354-366.
[12]Kouroku Y,Fujita E,Tanida I,et al.ER stress(PERK/eIF2alpha phosphorylation)mediates the polyglutamine-induced LC3 conversion,an essential step for autophagy formation[J].Cell Death Differ,2007,14(2):230-239.
[13]Momoi T.Conformational diseases and ER stress-mediated cell death:apoptotic cell death and autophagic cell death[J].Curr Mol Med,2006,6(1):111-118.
[14]Ding WX,Ni HM,Gao W,et al.LinKing of autophagy to ubiquitin-proteasome system is important for the regulation of endoplasmic reticulum stress and cell viability[J].Am J P athol,2007,171(2):513-524.
[15]Grotemeier A,Alers S,Pfisterer SG,et al.AMPK-independent induction of autophagy by cytosolic Ca2+ increase[J].Cell Signal,2010,22(6):914-925.
[16]Zalckvar E,Berissi H,Mizrachy L,et al.DAP-kinase-mediated phosphorylation on the BH3 domain of beclin 1 promotes dissociation of beclin 1 from Bcl-XL and induction of autophagy[J].EMBO Rep,2009,10(3): 285-292.
[17]Yoon SY,Ha YE,Choi JE,et al.Coxsackievirus B4 uses autophagy for replication after calpain activation in rat primary neurons[J].J Virol,2008,82(23):11976-11978.
[18]Robinson SM,Tsueng G,Sin J,et al.Coxsackievirus B exits the host cell in shed microvesicles displaying autophagosomal markers[J].PLoS Pathoq,2014,10(4):1-20
[19]B chir W, Maurin AC,Carraro V,et al.The eIF2α/ATF4 pathway is essential for stress-induced autophagy gene expression[J].Nucleic Acids Res,2013,41(16):7683-7699.
[20]Axe EL,Walker SA,Manifava M,et al.Autophagosome formation from membrane compartments enriched in phosphatidylinositol 3-phosphate and dynamically connected to the endoplasmic reticulum[J].Cell Biol,2008,182(4):685-701.
[21]Khakpoor A,Panyasrivanit M,Wikan N,et al.A role for autophagolysosome in dengue virus 3 production in HepG2 cell[J].J Gen Virol,2009,90(Pt 5):1093-1103.
[22]Ursu ON,Sauter M,Ettischer N,et al.Heme oxygenase-1 mediates oxidative stress and apoptosis in coxsackievirus B3-induced myocarditis[J].Cell Physiol Biochem,2014,33(1):52-66.
[23]Li YC,Ge LS,Yang PL,et al.Carvedilol treatment ameliorates acute coxsackievirus B3-induced myocarditis associated with oxidative stress reduction[J].Eur J Pharmacol,2010,640(25):1-3.
[24]赵德超,高新宇,余首先,等.1,6二磷酸果糖对病毒性心肌炎小鼠NADPH氧化酶P22亚基的影响[J].中国地方病学杂志,2013,32(1):50-53.
[25]Lipinski MM,Zheng B,Lu T,et al.Genome-wide analysis reveals mechanisms modulating autophagy in normal brain aging and in Alzheimer‘s disease[J].Proc Natl Acad Sci,2010,107(32):14164-14169.
[26]Xu YN,Cui XS,Sun SC,et al.Mitochondrial dysfunction inflences apoptosis and autophagy in porcine parthenotes developing in vitro[J].J Reprod Dev,2011,57(1):143-150.
[27]Kim I,Rodriguec-Enriquez S,Lemasters JJ.Selective degradation of mitochondria by mitophagy[J].Arch Biochem Biophys,2007,462(2):245-253.
[28]Kaushik S,Cuervo AM.Autophagy as a cell-repair mechanism: activation of chaperone mediated autophagy during oxidative stress[J].Mola spects Med,2006,27(5-6):444-454.

备注/Memo

备注/Memo:
收稿日期:2015-01-24.
基金项目:黑龙江省自然科学基金资助(D201070)
通讯作者:赵德超,主任医师,主要从事病毒性心肌炎发病机制的研究 Email:drzhaodechao@163.com
作者简介:于建才,硕士生 Email:xiwangyjc@163.com
更新日期/Last Update: 2016-04-25