心肌细胞超微结构改变与心力衰竭
戚艳超,徐明
摘要(Abstract):
心肌细胞是心脏收缩和舒张的基本结构单元,由肌膜/横管、肌质网、肌纤维、线粒体、细胞核等多种细胞器构成。心肌细胞及其亚细胞结构是维持心脏正常工作的结构基础。在多种原因所致的心脏重塑发生时,这些结构出现了一系列的改变,导致心脏舒缩功能紊乱,并进一步加重重塑,最终导致心力衰竭的发生。因此,了解心肌细胞及其亚细胞结构在心力衰竭发展过程中的变化及其调控机制对心力衰竭的早期诊断和治疗具有重要的意义。本文将就此作一简要综述。
关键词(KeyWords): 心肌细胞超微结构;心力衰竭
基金项目(Foundation): 国家自然科学基金项目(81070196);; 教育部新世纪优秀人才项目(BMU20100012)
作者(Author): 戚艳超,徐明
参考文献(References):
- [1]Wei S,Guo A,Chen B,et al.T-tubule remodeling during transition from hypertrophy to heart failure[J].Circ Res,2010,107(4):520-531.
- [2]Wu HD,Xu M,Li RC,et al.Ultrastructural remodelling of Ca(2+)signalling apparatus in failing heart cells[J].Cardiovasc Res,2012,95(4):430-438.
- [3]Zhang HB,Li RC,Xu M,et al.Ultrastructural uncoupling between T-tubules and sarcoplasmic reticulum in human heart failure[J].Cardiovasc Res,2013.
- [4]Xu M,Zhou P,Xu SM,et al.Intermolecular failure of L-type Ca2+channel and ryanodine receptor signaling in hypertrophy[J].PLoS Biol,2007,5(2):e21.
- [5]Xu M,Wu HD,Li RC,et al.Mir-24regulates junctophilin-2expression in cardiomyocytes[J].Circ Res,2012,111(7):837-841.
- [6]Li RC,Tao J,Guo YB,et al.In vivo suppression of microRNA-24prevents the transition toward decompensated hypertrophy in aortic-constricted mice[J].Circ Res,2013,112(4):601-605.
- [7]Hein S,Scholz D,Fujitani N,et al.Altered expression of titin and contractile proteins in failing human myocardium[J].J Mol Cell Cardiol,1994,26(10):1291-1306.
- [8]Person V,Kostin S,Suzuki K,et al.Antisense oligonucleotide experiments elucidate the essential role of titin in sarcomerogenesis in adult rat cardiomyocytes in long-term culture[J].J Cell Sci,2000,113(Pt21):3851-3859.
- [9]Ellis CE,Naicker D,Basson KM,et al.Damage to some contractile and cytoskeleton proteins of the sarcomere in rat neonatal cardiomyocytes after exposure to pavetamine[J].Toxicon,2010,55(6):1071-1079.
- [10]Hamdani N,Krysiak J,Kreusser MM,et al.Crucial role for Ca2+/calmodulin-dependent protein kinase-ii in regulating diastolic stress of normal and failing hearts via titin phosphorylation[J].Circ Res,2013,112(4):664-674.
- [11]Schaper J,Kostin S,Hein S,et al.Structural remodelling in heart failure[J].Exp Clin Cardiol,2002,7(2-3):64-68.
- [12]Huang J,Min Lu M,Cheng L,et al.Myocardin is required for cardiomyocyte survival and maintenance of heart function[J].Proc Natl Acad Sci U S A,2009,106(44):18734-18739.
- [13]Sharov VG,Todor AV,Silverman N,et al.Abnormal mitochondrial respiration in failed human myocardium[J].J Mol Cell Cardiol,2000,32(12):2361-2367.
- [14]Leung AW,Halestrap AP.Recent progress in elucidating themolecular mechanism of the mitochondrial permeability transition pore[J].Biochim Biophys Acta,2008,1777(7-8):946-952.
- [15]Javadov S,Karmazyn M,Escobales N.Mitochondrial permeability transition pore opening as a promising therapeutic target in cardiac diseases[J].J Pharmacol Exp Ther,2009,330(3):670-678.
- [16]Elrod JW,Wong R,Mishra S,et al.Cyclophilin D controls mitochondrial pore-dependent Ca(2+)exchange,metabolic flexibility,and propensity for heart failure in mice[J].J Clin Invest,2010,120(10):3680-3687.
- [17]Huang X,Sun L,Ji S,et al.Kissing and nanotunneling mediate intermitochondrial communication in the heart[J].Proc Natl Acad Sci U S A,2013,110(8):2846-2851.
- [18]Cortés R,Roselló-LletíE,Rivera M,et al.Influence of heart failure on nucleocytoplasmic transport in human cardiomyocytes[J].Cardiovasc Res,2010,85(3):464-472.
- [19]Tarazón E,Rivera M,Roselló-LletíE,et al.Heart failure induces significant changes in nuclear pore complex of human cardiomyocytes[J].PLoS One,2012,7(11):e48957.