[1]钟祯 张霄旦 李万根.内质网与线粒体相互作用在糖尿病心肌病中的作用[J].国际内分泌代谢杂志,2019,39(01):57-60.[doi:10.3760/cma.j.issn.1673-4157.2019.01.014]
　Zhong Zhen,Zhang Xiaodan,Li Wangen.Roles of the interactions between endoplasmic reticulum and mitochondria in diabetic cardiomyopathy[J].International Journal of Endocrinology and Metabolism,2019,39(01):57-60.[doi:10.3760/cma.j.issn.1673-4157.2019.01.014]
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内质网与线粒体相互作用在糖尿病心肌病中的作用()
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《国际内分泌代谢杂志》[ISSN:1673-4157/CN:12-1383/R]

卷:
39
期数:
2019年01期
页码:
57-60
栏目:
综述
出版日期:
2019-01-20

文章信息/Info

Title:
Roles of the interactions between endoplasmic reticulum and mitochondria in diabetic cardiomyopathy
作者:
钟祯 张霄旦 李万根
广州医科大学附属第二医院 510260
Author(s):
Zhong Zhen;  Zhang Xiaodan;  Li Wangen
Department of Endocrinology, The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou 510260, China Corresponding author: Li Wangen, Email:liwg660@126.com
关键词:
糖尿病心肌病;  线粒体;  内质网;  线粒体结合内质网膜
Keywords:
Diabetic cardiomyopathy;  Mitochondria;  Endoplasmic reticulum;  Mitochondria-associated endoplasmic reticulum membranes
DOI:
10.3760/cma.j.issn.1673-4157.2019.01.014
摘要:
糖尿病心肌病一种独立于高血压、冠心病等疾病的特异性心肌病变,是2型糖尿病患者致死的主要原因,但目前糖尿病心肌病的发病机制尚未完全阐明。内质网和线粒体是细胞内重要的细胞器,参与细胞各项生命活动,这两种细胞器间的相互作用与细胞内各种信号转导密切相关。最近一些研究表明,高糖可致细胞内内质网与线粒体连接松散,相互作用减弱,内质网与线粒体之间相互作用的变化可通过调节内质网应激、细胞缺氧应激、Ca2+稳态等,参与糖尿病心肌病的发生、发展。
Abstract:
Diabetic cardiomyopathy is one of the main causes of death in patients with type 2 diabetes mellitus, which is independent of hypertension and coronary heart disease. However, the pathogenesis of diabetic cardiomyopathy has not been fully elucidated yet. Endoplasmic reticulum and mitochondria are important intracellular organelles involved in cellular activities. The interactions between these two organelles are closely correlated with various cell signaling pathways. Recent studies have shown that high glucose can lose the interaction between endoplasmic reticulum and mitochondria. The change of the interactions between endoplasmic reticulum and mitochondria are involved in the development of diabetic cardiomyopathy by regulating endoplasmic reticulum stress, cellular hypoxia stress, and Ca2+ homeostasis.

参考文献/References:

[1] Wang L,Gao P,Zhang M,et al.Prevalence and ethnic pattern of diabetes and prediabetes in China in 2013[J].JAMA,2017,317(24):2515-2523.DOI:10.1001/jama.2017.7596.
[2] Pappachan JM,Varughese GI,Sriraman R,et al.Diabetic cardiomyopathy:pathophysiology, diagnostic evaluation and management[J].World J Diabetes,2013,4(5):177-189.DOI:10.4239/wjd.v4.i5.177.
[3] Rubler S,Dlugash J,Yuceoglu YZ,et al.New type of cardiomyopathy associated with diabetic glomerulosclerosis[J].Am J Cardiol,1972,30(6):595-602.
[4] Marchi S,Patergnani S,Pinton P.The endoplasmic reticulum-mitochondria connection: one touch, multiple functions[J].Biochim Biophys Acta,2014,1837(4):461-469.DOI:10.1016/j.bbabio.2013.10.015.
[5] Vance JE.Phospholipid synthesis in a membrane fraction associated with mitochondria[J].J Biol Chem,1990,265(13):7248-7256.
[6] Phillips MJ,Voeltz GK.Structure and function of ER membrane contact sites with other organelles[J].Nat Rev Mol Cell Biol,2016,17(2):69-82.DOI:10.1038/nrm.2015.8.
[7] Csordás G,Renken C,Várnai P,et al.Structural and functional features and significance of the physical linkage between ER and mitochondria[J].J Cell Biol,2006,174(7):915-921.DOI:10.1083/jcb.200604016.
[8] Ozcan L,Tabas I. Calcium signalling and ER stress in insulin resistance and atherosclerosis[J].J Intern Med,2016,280(5):457-464.DOI:10.1111/joim.12562.
[9] Mun～oz JP,Ivanova S,Sánchez-Wandelmer J,et al.Mfn2 modulates the UPR and mitochondrial function via repression of PERK[J].EMBO J,2013,32(17):2348-2361.DOI:10.1038/emboj.2013.168.
[10] Gao Q,Wang XM,Ye HW,et al.Changes in the expression of cardiac mitofusin-2 in different stages of diabetes in rats[J].Mol Med Rep,2012,6(4):811-814.DOI:10.3892/mmr.2012.1002.
[11] Yang F,Yu X,Li T,et al.Exogenous H2S regulates endoplasmic reticulum-mitochondria cross-talk to inhibit apoptotic pathways in STZ-induced type Ⅰ diabetes[J].Am J Physiol Endocrinol Metab,2017,312(3):E190-E203.DOI:10.1152/ajpendo.00196.2016.
[12] Chen M,Chen Z,Wang Y,et al.Mitophagy receptor FUNDC1 regulates mitochondrial dynamics and mitophagy[J].Autophagy,2016,12(4):689-702.DOI:10.1080/15548627.2016.1151580.
[13] Wu W,Lin C,Wu K,et al.FUNDC1 regulates mitochondrial dynamics at the ER-mitochondrial contact site under hypoxic conditions[J].EMBO J,2016,35(13):1368-1384.DOI:10.15252/embj.201593102.
[14] Verfaillie T,Rubio N,Garg AD,et al.PERK is required at the ER-mitochondrial contact sites to convey apoptosis after ROS-based ER stress[J].Cell Death Differ,2012,19(11):1880-1891.DOI:10.1038/cdd.2012.74.
[15] Liu ZW,Zhu HT,Chen KL,et al.Protein kinase RNA-like endoplasmic reticulum kinase(PERK)signaling pathway plays a majorrole in reactive oxygen species(ROS)-mediated endoplasmic reticulum stress-inducedapoptosis in diabetic cardiomyopathy[J].Cardiovasc Diabetol,2013,12:158.DOI:10.1186/1475-2840-12-158.
[16] Kumar S,Kain V,Sitasawad SL.High glucose-induced Ca2+ overload and oxidative stress contribute to apoptosis of cardiac cells through mitochondrial dependent and independent pathways[J].Biochim Biophys Acta,2012,1820(7):907-920.DOI:10.1016/j.bbagen.2012.02.010.
[17] Rizzuto R,Pinton P,Carrington W,et al. Close contacts with the endoplasmic reticulum as determinants of mitochondrial Ca2+ responses[J].Science,1998,280(5370):1763-1766.
[18] Thoudam T,Jeon JH,Ha CM,et al.Role of mitochondria-associated endoplasmic reticulum membrane in inflammation-mediated metabolic diseases[J].Mediators Inflamm,2016,2016:1851420.DOI:10.1155/2016/1851420.
[19] Min CK,Yeom DR,Lee KE,et al.Coupling of ryanodine receptor 2 and voltage-dependent anion channel 2 is essential for Ca2+ transfer from the sarcoplasmic reticulum to the mitochondria in the heart[J].Biochem J,2012,447(3):371-379.DOI:10.1042/BJ20120705.
[20] Theurey P,Tubbs E,Vial G,et al.Mitochondria-associated endoplasmic reticulum membranes allow adaptation of mitochondrial metabolism to glucose availability in the liver[J].J Mol Cell Biol,2016,8(2):129-143.DOI:10.1093/jmcb/mjw004.

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备注/Memo

备注/Memo:
通信作者:李万根,Email:liwg660@126.com
基金项目:广东省自然科学基金(2017A030310257); 广州市科技计划项目(201707010045); 广州市医药卫生科技项目(20171A011299); 广州医科大学博士、留学回国人员科研项目(2015C10)
Fund program:Natural Science Foundation of Guangdong Province of China(2017A030310257); Science and Technology Program of Guangzhou of China(201707010045); The Project of Medical and Health Science and Technology of Guangzhou(20171A011299); Scientific Research Program for Doctor and Returned Students of Guangzhou Medical University(2015C10)
更新日期/Last Update: 2019-01-20