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Science China Life Sciences

, Volume 59, Issue 8, pp 770–776

First Online: 19 July 2016Received: 16 May 2015Accepted: 07 June 2016DOI: 10.1007-s11427-016-5089-3

Cite this article as: Zhou, J., Dhakal, K. & Yi, J. Sci. China Life Sci. 2016 59: 770. doi:10.1007-s11427-016-5089-3

Abstract

Muscle uses Ca as a messenger to control contraction and relies on ATP to maintain the intracellular Ca homeostasis. Mitochondria are the major sub-cellular organelle of ATP production. With a negative inner membrane potential, mitochondria take up Ca from their surroundings, a process called mitochondrial Ca uptake. Under physiological conditions, Ca uptake into mitochondria promotes ATP production. Excessive uptake causes mitochondrial Ca overload, which activates downstream adverse responses leading to cell dysfunction. Moreover, mitochondrial Ca uptake could shape spatio-temporal patterns of intracellular Ca signaling. Malfunction of mitochondrial Ca uptake is implicated in muscle degeneration. Unlike non-excitable cells, mitochondria in muscle cells experience dramatic changes of intracellular Ca levels. Besides the sudden elevation of Ca level induced by action potentials, Ca transients in muscle cells can be as short as a few milliseconds during a single twitch or as long as minutes during tetanic contraction, which raises the question whether mitochondrial Ca uptake is fast and big enough to shape intracellular Ca signaling during excitation-contraction coupling and creates technical challenges for quantification of the dynamic changes of Ca inside mitochondria. This review focuses on characterization of mitochondrial Ca uptake in skeletal muscle and its role in muscle physiology and diseases.

Keywordsskeletal muscle mitochondria Ca This article is published with open access at link.springer.com

Open Access This article is distributed under the terms of the Creative Commons Attribution License which permits any use, distribution, and reproduction in any medium, provided the original authors and source are credited.

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Author: Jingsong Zhou - Kamal Dhakal - Jianxun Yi

Source: https://link.springer.com/







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