线粒体损伤与动脉粥样硬化的研究进展
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摘要
线粒体是细胞的能量工厂,是一种高度动态的双层膜细胞器,广泛分布于机体的多种细胞类型。很多研究表明,线粒体不仅在维持细胞能量稳态中起着重要作用,还参与对钙离子信号传递、细胞增殖和分化的调节。新近研究表明,线粒体损伤参与动脉粥样硬化的发生发展。本文综述了线粒体损伤与动脉粥样硬化的新进展,以期为动脉粥样硬化的有效防治提供新的策略和靶点。
Mitochondria are the power house of the cell, which is a highly dynamic double-membrane-bound organelle that is widely distributed in many cell types. Many studies have shown that mitochondria not only play a key role in maintaining cellular energy homeostasis, but also participate in the regulation of calcium signal transduction, cell proliferation and differentiation. Recent studies have shown that mitochondrial injury is involved in the initiation and progression of atherosclerosis. In this review, we have analyzed the recent advances in mitochondrial injury and atherosclerosis, in order to provide new strategies and targets for the effective prevention and therapy of atherosclerotic lesions.
Mitochondria are the power house of the cell, which is a highly dynamic double-membrane-bound organelle that is widely distributed in many cell types. Many studies have shown that mitochondria not only play a key role in maintaining cellular energy homeostasis, but also participate in the regulation of calcium signal transduction, cell proliferation and differentiation. Recent studies have shown that mitochondrial injury is involved in the initiation and progression of atherosclerosis. In this review, we have analyzed the recent advances in mitochondrial injury and atherosclerosis, in order to provide new strategies and targets for the effective prevention and therapy of atherosclerotic lesions.
引文
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[27]Childs BG,Baker DJ,Wijshake T,et al.Senescent intimal foam cells are deleterious at all stages of atherosclerosis.Science,2016,354(6311):472-477
[28]Liu LP,Cheng K,Ning MA,et al.Association between peripheral blood cells mitochondrial DNA content and severity of coronary heart disease.Atherosclerosis,2017,261:105-110
[29]Yu EPK,Reinhold J,Yu H,et al.Mitochondrial respiration is reduced in atherosclerosis,promoting necrotic core formation and reducing relative fibrous cap thickness.Arterioscler Thromb Vasc Biol,2017,37(12):2322-2332
[30]曾召林,陈姣姣,马小峰,等.细胞焦亡在动脉粥样硬化中的作用.生命的化学,2018,38(3):464-472
[31]Rottenberg H,Hoek JB.The path from mitochondrial ROS to aging runs through the mitochondrial permeability transition pore.Aging Cell,2017,16(5):943-955
[32]Zheng Y,Gardner SE,Clarke MC.Cell death,damage-associated molecular patterns,and sterile inflammation in cardiovascular disease.Arterioscler Thromb Vasc Biol,2011,31(12):2781-2786
[33]Wang J,Chen H,Liu Y,et al.Retinol binding protein 4induces mitochondrial dysfunction and vascular oxidative damage.Atherosclerosis,2015,240(2):335-344
[2]Zhang YK,Wang CY,Jin Y,et al.Activating the PGC-1α/TERT pathway by catalpol ameliorates atherosclerosis via modulating ROS production,DNA damage,and telomere function:Implications on mitochondria and telomere link.Oxid Med Cell Longev,2018,2018:2876350
[3]Safiedeen Z,Andriantsitohaina R,Martinez MC.Dialogue between endoplasmic reticulum and mitochondria as a key actor of vascular dysfunction associated to metabolic disorders.Int J Biochem Cell Biol,2016,77:10-14
[4]Jheng HF,Tsal PJ,Guo SM,et al.Mitochondrial fission contributes to mitochondrial dysfunction and insulin resistance in skeletal muscle.Mol Cell Biol,2012,32(2):309-319
[5]于海奕,郭艳红,高炜.线粒体融合蛋白2与心血管疾病.生理科学进展,2010,41(01):11-16.
[6]Zmijewski JW,Moellering DR,Le Goffe C,et al.Oxidized LDL induces mitochondrially associated reactive oxygen/nitrogen species formation in endothelial cells.Am J Physiol Heart Circ Physiol,2005,289(2):H852-861
[7]Rovira-Llopis S,Apostolova N,Banuls C,et al.Mitochondria,the NLRP3 inflammasome,and sirtuins in type2 diabetes:new therapeutic targets.Antioxid Redox Signal,2018,29(8):749-791
[8]Meyer A,Laverny G,Bernardi L,et al.Mitochondria:an organelle of bacterial origin controlling inflammation.Front Immunol,2018,9:536
[9]López-Doménech G,Covill-Cooke C,Ivankovic D,et al.Miro proteins coordinate microtubule-and actin-dependent mitochondrial transport and distribution.EMBO J,2018,37(3):321-336
[10]Wu X,Li L,Jiang H.Doa1 targets ubiquitinated substrates for mitochondria-associated degradation.J Cell Biol,2016,213(1):49-63
[11]Zhao G,Li G,Schindelin H,et al.An armadillo motif in Ufd3 interacts with Cdc48 and is involved in ubiquitin homeostasis and protein degradation.Proc Natl Acad Sci USA,2009,106(38):16197-16202
[12]Lavie J,De Belvalet H,Sonon S,et al.Ubiquitin-dependent degradation of mitochondrial proteins regulates energy metabolism.Cell Rep,2018,23(10):2852-2863
[13]Birch-Machin MA.The role of mitochondria in ageing and carcinogenesis.Clin Exp Dermatol,2006,31(4):548-552
[14]Nicholls DG.Power,sex,suicide-Mitochondria and the meaning of life.Science,2006,311(5769):1869-1869
[15]Weiss JN,Korge P,Honda HM,et al.Role of the mitochondrial permeability transition in myocardial disease.Circ Res,2003,93(4):292-301
[16]Marin-Garcia J,Goldenthal MJ.Mitochondria play a critical role in cardioprotection.J Card Fail,2004,10(1):55-66
[17]Ali MH,Pearlstein DP,Mathieu CE,et al.Mitochondrial requirement for endothelial responses to cyclic strain:implications for mechanotransduction.Am J Physiol Lung Cell Mol Physiol,2004,287(3):L486-496
[18]Rakhit RD,Mojet MH,Marber MS,et al.Mitochondria as targets for nitric oxide-induced protection during simulated ischemia and reoxygenation in isolated neonatal cardiomyocytes.Circulation,2001,103(21):2617-2623
[19]Yan XJ,Yu X,Wang XP,et al.Mitochondria play an important role in the cell proliferation suppressing activity of berberine.Sci Rep,2017,7:41712
[20]Nasrallah CM,Horvath TL.Mitochondrial dynamics in the central regulation of metabolism.Nat Rev Endocrinol,2014,10(11):650-658
[21]Daste F,Sauvanet C,Bavdek A,et al.The heptad repeat domain 1 of Mitofusin has membrane destabilization function in mitochondrial fusion.EMBO Rep,2018,19(6):pii:e43637
[22]Cao YL,Meng S,Chen Y,et al.MFN1 structures reveal nucleotide-triggered dimerization critical for mitochondrial fusion.Nature,2017,542(7641):372-376
[23]Scheede-Bergdahl C,Bergdahl A.Adaptation of mitochondrial expression and ATP production in dedifferentiating vascular smooth muscle cells.Can J Physiol Pharmacol,2017;95(12):1473-1479
[24]Docherty CK,Carswell A,Friel E,et al.Impaired mitochondrial respiration in human carotid plaque atherosclerosis:A potential role for Pink1 in vascular smooth muscle cell energetics.Atherosclerosis,2018,268:1-11
[25]Wang H,Robichaux WG,Wang Z,et al.Inhibition of Epac1 suppresses mitochondrial fission and reduces neointima formation induced by vascular injury.Sci Rep,2016,6:36552
[26]Wiley CD,Velarde MC,Lecot P,et al.Mitochondrial dysfunction induces senescence with a distinct secretory phenotype.Cell Metab,2016,23(2):303-314
[27]Childs BG,Baker DJ,Wijshake T,et al.Senescent intimal foam cells are deleterious at all stages of atherosclerosis.Science,2016,354(6311):472-477
[28]Liu LP,Cheng K,Ning MA,et al.Association between peripheral blood cells mitochondrial DNA content and severity of coronary heart disease.Atherosclerosis,2017,261:105-110
[29]Yu EPK,Reinhold J,Yu H,et al.Mitochondrial respiration is reduced in atherosclerosis,promoting necrotic core formation and reducing relative fibrous cap thickness.Arterioscler Thromb Vasc Biol,2017,37(12):2322-2332
[30]曾召林,陈姣姣,马小峰,等.细胞焦亡在动脉粥样硬化中的作用.生命的化学,2018,38(3):464-472
[31]Rottenberg H,Hoek JB.The path from mitochondrial ROS to aging runs through the mitochondrial permeability transition pore.Aging Cell,2017,16(5):943-955
[32]Zheng Y,Gardner SE,Clarke MC.Cell death,damage-associated molecular patterns,and sterile inflammation in cardiovascular disease.Arterioscler Thromb Vasc Biol,2011,31(12):2781-2786
[33]Wang J,Chen H,Liu Y,et al.Retinol binding protein 4induces mitochondrial dysfunction and vascular oxidative damage.Atherosclerosis,2015,240(2):335-344