The Involvement of Mg2+ in Regulation of Cellular and Mitochondrial Functions

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Abstract

Mg ²⁺ is an essential mineral with pleotropic impacts on cellular physiology and functions. It acts as a cofactor of several important enzymes, as a regulator of ion channels such as voltage-dependent Ca ²⁺ channels and K ⁺ channels and on Ca ²⁺-binding proteins. In general, Mg ²⁺ is considered as the main intracellular antagonist of Ca ²⁺, which is an essential secondary messenger initiating or regulating a great number of cellular functions. This review examines the effects of Mg ²⁺ on mitochondrial functions with a particular focus on energy metabolism, mitochondrial Ca ²⁺ handling, and apoptosis.

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Most cited references 84

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Calcium signaling.

David E Clapham, Md. Islam (2008)

Calcium ions (Ca(2+)) impact nearly every aspect of cellular life. This review examines the principles of Ca(2+) signaling, from changes in protein conformations driven by Ca(2+) to the mechanisms that control Ca(2+) levels in the cytoplasm and organelles. Also discussed is the highly localized nature of Ca(2+)-mediated signal transduction and its specific roles in excitability, exocytosis, motility, apoptosis, and transcription.

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Mitochondria as sensors and regulators of calcium signalling.

Rosario Rizzuto, Diego De Stefani, Anna Raffaello … (2012)

During the past two decades calcium (Ca(2+)) accumulation in energized mitochondria has emerged as a biological process of utmost physiological relevance. Mitochondrial Ca(2+) uptake was shown to control intracellular Ca(2+) signalling, cell metabolism, cell survival and other cell-type specific functions by buffering cytosolic Ca(2+) levels and regulating mitochondrial effectors. Recently, the identity of mitochondrial Ca(2+) transporters has been revealed, opening new perspectives for investigation and molecular intervention.

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NCLX is an essential component of mitochondrial Na+/Ca2+ exchange.

Raz Palty, William Silverman, Michal Hershfinkel … (2010)

Mitochondrial Ca(2+) efflux is linked to numerous cellular activities and pathophysiological processes. Although it is established that an Na(+)-dependent mechanism mediates mitochondrial Ca(2+) efflux, the molecular identity of this transporter has remained elusive. Here we show that the Na(+)/Ca(2+) exchanger NCLX is enriched in mitochondria, where it is localized to the cristae. Employing Ca(2+) and Na(+) fluorescent imaging, we demonstrate that mitochondrial Na(+)-dependent Ca(2+) efflux is enhanced upon overexpression of NCLX, is reduced by silencing of NCLX expression by siRNA, and is fully rescued by the concomitant expression of heterologous NCLX. NCLX-mediated mitochondrial Ca(2+) transport was inhibited, moreover, by CGP-37157 and exhibited Li(+) dependence, both hallmarks of mitochondrial Na(+)-dependent Ca(2+) efflux. Finally, NCLX-mediated mitochondrial Ca(2+) exchange is blocked in cells expressing a catalytically inactive NCLX mutant. Taken together, our results converge to the conclusion that NCLX is the long-sought mitochondrial Na(+)/Ca(2+) exchanger.

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Author and article information

Journal

Journal ID (nlm-ta): Oxid Med Cell Longev

Journal ID (iso-abbrev): Oxid Med Cell Longev

Journal ID (publisher-id): OMCL

Title: Oxidative Medicine and Cellular Longevity

Publisher: Hindawi

ISSN (Print): 1942-0900

ISSN (Electronic): 1942-0994

Publication date (Print): 2017

Publication date (Electronic): 5 July 2017

Volume: 2017

Electronic Location Identifier: 6797460

Affiliations

Biomedical Center Martin JFM CU and Department of Medical Biochemistry JFM CU, Jessenius Faculty of Medicine in Martin (JFM CU), Comenius University in Bratislava, Martin, Slovakia

Author notes

*Peter Racay: racay@ 123456jfmed.uniba.sk

Academic Editor: Rhian Touyz

Author information

Peter Racay http://orcid.org/0000-0003-2166-1556

Article

DOI: 10.1155/2017/6797460

PMC ID: 5516748

PubMed ID: 28757913

SO-VID: 7ddb2ebe-6c29-4e36-ae69-d3e4ae56fd04

License:

This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

History

Date received : 24 March 2017

Date accepted : 31 May 2017

Funding

Funded by: European Regional Development Fund

Funded by: Creating a New Diagnostic Algorithm for Selected Cancer Diseases

Award ID: 26220220022

Funded by: Biomedical Center Martin

Award ID: 26220220187

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