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横纹肌亚细胞器之间的能量相互作用。

Energetic Interactions Between Subcellular Organelles in Striated Muscles.

作者信息

Piquereau Jérôme, Veksler Vladimir, Novotova Marta, Ventura-Clapier Renée

机构信息

Université Paris-Saclay, Inserm, UMR-S 1180, Châtenay-Malabry, France.

Department of Cellular Cardiology, Biomedical Research Center, Institute of Experimental Endocrinology, Slovak Academy of Sciences, Bratislava, Slovakia.

出版信息

Front Cell Dev Biol. 2020 Oct 2;8:581045. doi: 10.3389/fcell.2020.581045. eCollection 2020.

DOI:10.3389/fcell.2020.581045
PMID:33134298
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7561670/
Abstract

Adult striated muscle cells present highly organized structure with densely packed intracellular organelles and a very sparse cytosol accounting for only few percent of cell volume. These cells have a high and fluctuating energy demand that, in continuously working oxidative muscles, is fulfilled mainly by oxidative metabolism. ATP produced by mitochondria should be directed to the main energy consumers, ATPases of the excitation-contraction system; at the same time, ADP near ATPases should rapidly be eliminated. This is achieved by phosphotransfer kinases, the most important being creatine kinase (CK). Specific CK isoenzymes are located in mitochondria and in close proximity to ATPases, forming efficient energy shuttle between these structures. In addition to phosphotransfer kinases, ATP/ADP can be directly channeled between mitochondria co-localized with ATPases in a process called "direct adenine nucleotide channeling, DANC." This process is highly plastic so that inactivation of the CK system increases the participation of DANC to energy supply owing to the rearrangement of cell structure. The machinery for DANC is built during postnatal development in parallel with the increase in mitochondrial mass, organization, and complexification of the cell structure. Disorganization of cell architecture remodels the mitochondrial network and decreases the efficacy of DANC, showing that this process is intimately linked to cardiomyocyte structure. Accordingly, in heart failure, disorganization of the cell structure along with decrease in mitochondrial mass reduces the efficacy of DANC and together with alteration of the CK shuttle participates in energetic deficiency contributing to contractile failure.

摘要

成年横纹肌细胞呈现出高度有组织的结构,细胞内细胞器密集排列,细胞质非常稀疏,仅占细胞体积的百分之几。这些细胞具有高且波动的能量需求,在持续工作的氧化型肌肉中,主要通过氧化代谢来满足。线粒体产生的ATP应导向兴奋收缩系统的主要能量消耗者——ATP酶;与此同时,ATP酶附近的ADP应迅速被清除。这通过磷酸转移激酶来实现,其中最重要的是肌酸激酶(CK)。特定的CK同工酶位于线粒体中以及与ATP酶紧邻的位置,在这些结构之间形成高效的能量穿梭。除了磷酸转移激酶外,ATP/ADP还可以在与ATP酶共定位的线粒体之间直接进行通道运输,这一过程称为“直接腺嘌呤核苷酸通道运输,DANC”。这个过程具有高度可塑性,因此CK系统失活会由于细胞结构的重新排列而增加DANC对能量供应的参与度。DANC机制在出生后发育过程中与线粒体质量的增加、细胞结构的组织化和复杂化并行构建。细胞结构的紊乱会重塑线粒体网络并降低DANC的功效,表明这一过程与心肌细胞结构密切相关。因此,在心力衰竭中,细胞结构的紊乱以及线粒体质量的减少会降低DANC的功效,并与CK穿梭的改变一起参与导致收缩功能衰竭的能量缺乏。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fcf2/7561670/1dcb4f85db90/fcell-08-581045-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fcf2/7561670/7761e9e2c0c3/fcell-08-581045-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fcf2/7561670/1dcb4f85db90/fcell-08-581045-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fcf2/7561670/7761e9e2c0c3/fcell-08-581045-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fcf2/7561670/1dcb4f85db90/fcell-08-581045-g002.jpg

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本文引用的文献

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PLoS One. 2019 Apr 9;14(4):e0214740. doi: 10.1371/journal.pone.0214740. eCollection 2019.
2
Cardiomyocyte substructure reverts to an immature phenotype during heart failure.在心力衰竭过程中心肌细胞亚结构恢复为未成熟表型。
J Physiol. 2019 Apr;597(7):1833-1853. doi: 10.1113/JP277273. Epub 2019 Feb 27.
3
SR-mitochondria communication in adult cardiomyocytes: A close relationship where the Ca has a lot to say.
ACS Chem Biol. 2021 Nov 19;16(11):2202-2211. doi: 10.1021/acschembio.1c00350. Epub 2021 Oct 21.
4
Metabolic Basis of Creatine in Health and Disease: A Bioinformatics-Assisted Review.健康与疾病中的肌酸代谢基础:生物信息学辅助综述。
Nutrients. 2021 Apr 9;13(4):1238. doi: 10.3390/nu13041238.
成年心肌细胞中线粒体的 SR 通讯:一种密切的关系,其中 Ca 有很多话要说。
Arch Biochem Biophys. 2019 Mar 15;663:259-268. doi: 10.1016/j.abb.2019.01.026. Epub 2019 Jan 24.
4
The creatine kinase system as a therapeutic target for myocardial ischaemia-reperfusion injury.肌酸激酶系统作为心肌缺血再灌注损伤的治疗靶点。
Biochem Soc Trans. 2018 Oct 19;46(5):1119-1127. doi: 10.1042/BST20170504. Epub 2018 Sep 20.
5
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Front Physiol. 2018 Jul 19;9:959. doi: 10.3389/fphys.2018.00959. eCollection 2018.
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7
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