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心脏中的线粒体网络。

Mitochondrial network in the heart.

机构信息

Division of Cardiovascular Research, State Key Laboratory of Biomembrane and Membrane Biotechnology, Institute of Zoology, Chinese Academy of Sciences, Beijing, China.

出版信息

Protein Cell. 2012 Jun;3(6):410-8. doi: 10.1007/s13238-012-2921-9. Epub 2012 Jul 1.

DOI:10.1007/s13238-012-2921-9
PMID:22752872
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4875487/
Abstract

Mitochondria are subcellular organelles that provide energy for the cell. They form a dynamic tubular network and play an important role in maintaining the cell function and integrity. Heart is a powerful organ that supplies the motivation for circulation, thereby requiring large amounts of energy. Thus, the healthiness of cardiomyocytes and mitochondria is necessary for the normal cardiac function. Mitochondria not only lie in the center of the cell apoptotic pathway, but also are the major source of reactive oxygen species (ROS) generation. Mitochondrial morphological change includes fission and fusion that are regulated by a large number of proteins. In this review we discuss the regulators of mitochondrial fission/fusion and their association with cell apoptosis, autophagy and ROS production in the heart.

摘要

线粒体是为细胞提供能量的细胞器。它们形成一个动态的管状网络,在维持细胞功能和完整性方面发挥着重要作用。心脏是一个提供循环动力的强大器官,因此需要大量的能量。因此,心肌细胞和线粒体的健康对于心脏的正常功能是必要的。线粒体不仅位于细胞凋亡途径的中心,也是活性氧(ROS)产生的主要来源。线粒体的形态变化包括分裂和融合,它们受大量蛋白质的调节。在这篇综述中,我们讨论了线粒体分裂/融合的调节剂及其与心脏细胞凋亡、自噬和 ROS 产生的关系。

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本文引用的文献

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Regulation of acid-base transporters by reactive oxygen species following mitochondrial fragmentation.线粒体碎片化后活性氧对酸碱转运体的调节。
Am J Physiol Cell Physiol. 2012 Apr 1;302(7):C1045-54. doi: 10.1152/ajpcell.00411.2011. Epub 2012 Jan 11.
2
Autophagy proteins LC3B, ATG5 and ATG12 participate in quality control after mitochondrial damage and influence lifespan.自噬蛋白 LC3B、ATG5 和 ATG12 参与线粒体损伤后的质量控制,并影响寿命。
Autophagy. 2012 Jan;8(1):47-62. doi: 10.4161/auto.8.1.18174. Epub 2012 Jan 1.
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Mitochondrial fission in endothelial cells after simulated ischemia/reperfusion: role of nitric oxide and reactive oxygen species.模拟缺血/再灌注后内皮细胞中线粒体的分裂:一氧化氮和活性氧的作用。
Free Radic Biol Med. 2012 Jan 15;52(2):348-56. doi: 10.1016/j.freeradbiomed.2011.10.491. Epub 2011 Nov 6.
4
Cardiomyocyte deletion of mitofusin-1 leads to mitochondrial fragmentation and improves tolerance to ROS-induced mitochondrial dysfunction and cell death.肌细胞中线粒体融合蛋白 1 的缺失导致线粒体碎片化,并改善了对 ROS 诱导的线粒体功能障碍和细胞死亡的耐受能力。
Am J Physiol Heart Circ Physiol. 2012 Jan 1;302(1):H167-79. doi: 10.1152/ajpheart.00833.2011. Epub 2011 Oct 28.
5
Ionizing radiation accelerates Drp1-dependent mitochondrial fission, which involves delayed mitochondrial reactive oxygen species production in normal human fibroblast-like cells.电离辐射加速了依赖于 Drp1 的线粒体裂变,这涉及正常人类成纤维样细胞中线粒体活性氧的延迟产生。
Biochem Biophys Res Commun. 2011 Nov 4;414(4):795-800. doi: 10.1016/j.bbrc.2011.10.006. Epub 2011 Oct 7.
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Mitochondrial autophagy by Bnip3 involves Drp1-mediated mitochondrial fission and recruitment of Parkin in cardiac myocytes.Bnip3 通过 Drp1 介导线粒体分裂和 Parkin 的募集诱导心肌细胞中线粒体自噬。
Am J Physiol Heart Circ Physiol. 2011 Nov;301(5):H1924-31. doi: 10.1152/ajpheart.00368.2011. Epub 2011 Sep 2.
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Autofluorescence microscopy: a non-destructive tool to monitor mitochondrial toxicity.自发荧光显微镜:一种用于监测线粒体毒性的非破坏性工具。
Toxicol Lett. 2011 Oct 30;206(3):281-8. doi: 10.1016/j.toxlet.2011.06.025. Epub 2011 Jul 20.
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J Neurosci. 2011 Aug 3;31(31):11404-10. doi: 10.1523/JNEUROSCI.2223-11.2011.
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Nat Med. 2011 Jan;17(1):71-8. doi: 10.1038/nm.2282. Epub 2010 Dec 26.
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Mitochondria on guard: role of mitochondrial fusion and fission in the regulation of apoptosis.警惕的线粒体:线粒体融合与分裂在细胞凋亡调控中的作用
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