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From basic mechanisms to clinical applications in heart protection, new players in cardiovascular diseases and cardiac theranostics: meeting report from the third international symposium on "New frontiers in cardiovascular research".从心脏保护的基本机制到临床应用,心血管疾病和心脏诊疗学的新进展:第三届“心血管研究新前沿”国际研讨会会议报告
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J Physiol Biochem. 2016 Mar;72(1):83-91. doi: 10.1007/s13105-015-0460-6. Epub 2016 Jan 8.
3
Meeting report from the 2nd International Symposium on New Frontiers in Cardiovascular Research. Protecting the cardiovascular system from ischemia: between bench and bedside.第二届心血管研究新前沿国际研讨会会议报告。保护心血管系统免受缺血影响:从实验台到病床边。
Basic Res Cardiol. 2016 Jan;111(1):7. doi: 10.1007/s00395-015-0527-0. Epub 2015 Dec 14.
4
REMOTE ISCHEMIC CONDITIONING INFLUENCES MITOCHONDRIAL DYNAMICS.远程缺血预处理影响线粒体动力学。
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7
Akt protects the heart against ischaemia-reperfusion injury by modulating mitochondrial morphology.Akt通过调节线粒体形态来保护心脏免受缺血再灌注损伤。
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8
Atomic force and electron microscopic-based study of sarcolemmal surface of living cardiomyocytes unveils unexpected mitochondrial shift in heart failure.基于原子力和电子显微镜的活心肌细胞肌膜表面研究揭示了心力衰竭中意想不到的线粒体移位。
J Mol Cell Cardiol. 2014 Sep;74:162-72. doi: 10.1016/j.yjmcc.2014.05.006. Epub 2014 May 17.
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Physiological and structural differences in spatially distinct subpopulations of cardiac mitochondria: influence of cardiac pathologies.心脏线粒体在空间上不同亚群中的生理和结构差异:心脏病理学的影响。
Am J Physiol Heart Circ Physiol. 2014 Jul 1;307(1):H1-14. doi: 10.1152/ajpheart.00747.2013.
10
Acute inhibition of excessive mitochondrial fission after myocardial infarction prevents long-term cardiac dysfunction.急性抑制心肌梗死后过度的线粒体分裂可预防长期心功能障碍。
J Am Heart Assoc. 2013 Oct 8;2(5):e000461. doi: 10.1161/JAHA.113.000461.

心脏线粒体亚型的独特形态特征:缺血及缺血预处理的影响

Unique morphological characteristics of mitochondrial subtypes in the heart: the effect of ischemia and ischemic preconditioning.

作者信息

Kalkhoran Siavash Beikoghli, Munro Peter, Qiao Fan, Ong Sang-Bing, Hall Andrew R, Cabrera-Fuentes Hector, Chakraborty Bibhas, Boisvert William A, Yellon Derek M, Hausenloy Derek J

机构信息

Hatter Cardiovascular Institute, University College London, UK.

National Institute of Health Research University College London Hospitals Biomedical Research Ctr., UK.

出版信息

Discoveries (Craiova). 2017 Jan-Mar;5(1). doi: 10.15190/d.2017.1.

DOI:10.15190/d.2017.1
PMID:28736742
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5519153/
Abstract

RATIONALE

Three subsets of mitochondria have been described in adult cardiomyocytes - intermyofibrillar (IMF), subsarcolemmal (SSM), and perinuclear (PN). They have been shown to differ in physiology, but whether they also vary in morphological characteristics is unknown. Ischemic preconditioning (IPC) is known to prevent mitochondrial dysfunction induced by acute myocardial ischemia/reperfusion injury (IRI), but whether IPC can also modulate mitochondrial morphology is not known.

AIMS

Morphological characteristics of three different subsets of adult cardiac mitochondria along with the effect of ischemia and IPC on mitochondrial morphology will be investigated.

METHODS

Mouse hearts were subjected to the following treatments (N=6 for each group): stabilization only, IPC (3x5 min cycles of global ischemia and reperfusion), ischemia only (20 min global ischemia); and IPC and ischemia. Hearts were then processed for electron microscopy and mitochondrial morphology was assessed subsequently.

RESULTS

In adult cardiomyocytes, IMF mitochondria were found to be more elongated and less spherical than PN and SSM mitochondria. PN mitochondria were smaller in size when compared to the other two subsets. SSM mitochondria had similar area to IMF mitochondria but their sphericity measures were similar to PN mitochondria. Ischemia was shown to increase the sphericity parameters of all 3 subsets of mitochondria; reduce the length of IMF mitochondria, and increase the size of PN mitochondria. IPC had no effect on mitochondrial morphology either at baseline or after ischemia.

CONCLUSION

The three subsets of mitochondria in the adult heart are morphologically different. IPC does not appear to modulate mitochondrial morphology in adult cardiomyocytes.

摘要

理论依据

在成年心肌细胞中已描述了三种线粒体亚群——肌原纤维间(IMF)、肌膜下(SSM)和核周(PN)线粒体。它们在生理功能上已显示出差异,但在形态特征上是否也存在差异尚不清楚。已知缺血预处理(IPC)可预防急性心肌缺血/再灌注损伤(IRI)诱导的线粒体功能障碍,但IPC是否也能调节线粒体形态尚不清楚。

目的

研究成年心脏三种不同线粒体亚群的形态特征以及缺血和IPC对线粒体形态的影响。

方法

对小鼠心脏进行以下处理(每组N = 6):仅稳定状态、IPC(3个5分钟的全心缺血和再灌注周期)、仅缺血(20分钟全心缺血);以及IPC加缺血。然后对心脏进行处理以用于电子显微镜检查,并随后评估线粒体形态。

结果

在成年心肌细胞中,发现IMF线粒体比PN和SSM线粒体更长且更不呈球形。与其他两个亚群相比,PN线粒体尺寸更小。SSM线粒体的面积与IMF线粒体相似,但其球形度测量值与PN线粒体相似。缺血显示会增加所有3个线粒体亚群的球形度参数;缩短IMF线粒体的长度,并增加PN线粒体的大小。IPC在基线时或缺血后对线粒体形态均无影响。

结论

成年心脏中的三种线粒体亚群在形态上有所不同。IPC似乎不会调节成年心肌细胞中的线粒体形态。