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Compr Physiol. 2017 Mar 16;7(2):623-634. doi: 10.1002/cphy.c160013.

Calcium Transport and Signaling in Mitochondria.

Author information

1
Advanced Center for Chronic Diseases (ACCDiS), Faculty of Chemical and Pharmaceutical Sciences & Faculty of Medicine, University of Chile, Santiago, Chile.
2
Institute of Nutrition and Food Technology (INTA), University of Chile, Santiago, Chile.
3
Center for Molecular Studies of the Cell (CEMC), Institute of Biomedical Sciences (ICBM), Faculty of Medicine, University of Chile, Santiago, Chile.
4
Cardiology Division, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas, USA.

Abstract

Calcium (Ca2+) is a key player in the regulation of many cell functions. Just like Ca2+, mitochondria are ubiquitous, versatile, and dynamic players in determining both cell survival and death decisions. Given their ubiquitous nature, the regulation of both is deeply intertwined, whereby Ca2+ regulates mitochondrial functions, while mitochondria shape Ca2+ dynamics. Deregulation of either Ca2+ or mitochondrial signaling leads to abnormal function, cell damage or even cell death, thereby contributing to muscle dysfunction or cardiac pathologies. Moreover, altered mitochondrial Ca2+ homeostasis has been linked to metabolic diseases like cancer, obesity, and pulmonary hypertension. In this review article, we summarize the mechanisms that coordinate mitochondrial and Ca2+ responses and how they affect human health. © 2017 American Physiological Society. Compr Physiol 7:623-634, 2017.

PMID:
28333383
DOI:
10.1002/cphy.c160013
[Indexed for MEDLINE]

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