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心血管疾病中的线粒体机械传感器

Mitochondrial mechanosensor in cardiovascular diseases.

作者信息

Caffarra Malvezzi Cristina, Cabassi Aderville, Miragoli Michele

机构信息

Department of Medicine and Surgery, University of Parma, Parma, Italy.

Center of Excellence for Toxicological Research, Department of Medicine and Surgery, University of Parma, Parma, Italy.

出版信息

Vasc Biol. 2020 Jun 22;2(1):R85-R92. doi: 10.1530/VB-20-0002. eCollection 2020.

DOI:10.1530/VB-20-0002
PMID:32923977
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7439846/
Abstract

The role of mitochondria in cardiac tissue is of utmost importance due to the dynamic nature of the heart and its energetic demands, necessary to assure its proper beating function. Recently, other important mitochondrial roles have been discovered, namely its contribution to intracellular calcium handling in normal and pathological myocardium. Novel investigations support the fact that during the progression toward heart failure, mitochondrial calcium machinery is compromised due to its morphological, structural and biochemical modifications resulting in facilitated arrhythmogenesis and heart failure development. The interaction between mitochondria and sarcomere directly affect cardiomyocyte excitation-contraction and is also involved in mechano-transduction through the cytoskeletal proteins that tether together the mitochondria and the sarcoplasmic reticulum. The focus of this review is to briefly elucidate the role of mitochondria as (mechano) sensors in the heart.

摘要

由于心脏的动态特性及其能量需求,线粒体在心脏组织中的作用至关重要,这对于确保心脏正常跳动功能是必要的。最近,人们发现了线粒体的其他重要作用,即其在正常和病理心肌中对细胞内钙处理的贡献。新的研究支持这样一个事实,即在心力衰竭的进展过程中,线粒体钙机制由于其形态、结构和生化改变而受到损害,导致心律失常的易发性增加和心力衰竭的发展。线粒体与肌节之间的相互作用直接影响心肌细胞的兴奋 - 收缩,并且还通过将线粒体和肌浆网连接在一起的细胞骨架蛋白参与机械转导。本综述的重点是简要阐明线粒体作为心脏(机械)传感器的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa71/7439846/a3ef8c5288cf/VB-20-0002fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa71/7439846/9aa384c78d22/VB-20-0002fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa71/7439846/6a29e84c8458/VB-20-0002fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa71/7439846/fa3861f773ac/VB-20-0002fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa71/7439846/33f6915ecf82/VB-20-0002fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa71/7439846/a3ef8c5288cf/VB-20-0002fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa71/7439846/9aa384c78d22/VB-20-0002fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa71/7439846/6a29e84c8458/VB-20-0002fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa71/7439846/fa3861f773ac/VB-20-0002fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa71/7439846/33f6915ecf82/VB-20-0002fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa71/7439846/a3ef8c5288cf/VB-20-0002fig5.jpg

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Mitochondria as multifaceted regulators of cell death.线粒体作为细胞死亡的多面调节者。
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Cardiomyocyte-myofibroblast contact dynamism is modulated by connexin-43.心肌细胞-肌成纤维细胞接触动力受连接蛋白 43 调节。
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