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Annu Rev Biochem. 2016 Jun 2;85:161-92. doi: 10.1146/annurev-biochem-060614-034216. Epub 2016 May 4.

Enjoy the Trip: Calcium in Mitochondria Back and Forth.

Author information

1
Department of Biomedical Sciences, University of Padova, 35121 Padova, Italy; email: diego.destefani@unipd.it , rosario.rizzuto@unipd.it , tullio.pozzan@unipd.it.
2
National Research Council (CNR) Neuroscience Institute, 35121 Padova, Italy.
3
Venetian Institute of Molecular Medicine, 35121 Padova, Italy.

Abstract

In the last 5 years, most of the molecules that control mitochondrial Ca(2+) homeostasis have been finally identified. Mitochondrial Ca(2+) uptake is mediated by the Mitochondrial Calcium Uniporter (MCU) complex, a macromolecular structure that guarantees Ca(2+) accumulation inside mitochondrial matrix upon increases in cytosolic Ca(2+). Conversely, Ca(2+) release is under the control of the Na(+)/Ca(2+) exchanger, encoded by the NCLX gene, and of a H(+)/Ca(2+) antiporter, whose identity is still debated. The low affinity of the MCU complex, coupled to the activity of the efflux systems, protects cells from continuous futile cycles of Ca(2+) across the inner mitochondrial membrane and consequent massive energy dissipation. In this review, we discuss the basic principles that govern mitochondrial Ca(2+) homeostasis and the methods used to investigate the dynamics of Ca(2+) concentration within the organelles. We discuss the functional and structural role of the different molecules involved in mitochondrial Ca(2+) handling and their pathophysiological role.

KEYWORDS:

Ca2+ signaling; MCU complex; NCLX

[Indexed for MEDLINE]

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