» Articles » PMID: 24994533

The Destiny of Ca(2+) Released by Mitochondria

Overview
Journal J Physiol Sci
Specialty Physiology
Date 2014 Jul 5
PMID 24994533
Citations 37
Authors
Affiliations
Soon will be listed here.
Abstract

Mitochondrial Ca(2+) is known to regulate diverse cellular functions, for example energy production and cell death, by modulating mitochondrial dehydrogenases, inducing production of reactive oxygen species, and opening mitochondrial permeability transition pores. In addition to the action of Ca(2+) within mitochondria, Ca(2+) released from mitochondria is also important in a variety of cellular functions. In the last 5 years, the molecules responsible for mitochondrial Ca(2+) dynamics have been identified: a mitochondrial Ca(2+) uniporter (MCU), a mitochondrial Na(+)-Ca(2+) exchanger (NCLX), and a candidate for a mitochondrial H(+)-Ca(2+) exchanger (Letm1). In this review, we focus on the mitochondrial Ca(2+) release system, and discuss its physiological and pathophysiological significance. Accumulating evidence suggests that the mitochondrial Ca(2+) release system is not only crucial in maintaining mitochondrial Ca(2+) homeostasis but also participates in the Ca(2+) crosstalk between mitochondria and the plasma membrane and between mitochondria and the endoplasmic/sarcoplasmic reticulum.

Citing Articles

The multifaceted role of mitochondria in autism spectrum disorder.

Khaliulin I, Hamoudi W, Amal H Mol Psychiatry. 2024; 30(2):629-650.

PMID: 39223276 PMC: 11753362. DOI: 10.1038/s41380-024-02725-z.


Endoplasmic Reticulum and Mitochondrial Calcium Handling Dynamically Shape Slow Afterhyperpolarizations in Vasopressin Magnocellular Neurons.

Kirchner M, Althammer F, Campos-Lira E, Montanez J, Stern J J Neurosci. 2024; 44(30.

PMID: 38937101 PMC: 11270521. DOI: 10.1523/JNEUROSCI.0003-24.2024.


Cell-specific modulation of mitochondrial respiration and metabolism by the pro-apoptotic Bcl-2 family members Bax and Bak.

Sovilj D, Kelemen C, Dvorakova S, Zobalova R, Raabova H, Kriska J Apoptosis. 2023; 29(3-4):424-438.

PMID: 38001340 DOI: 10.1007/s10495-023-01917-2.


Sepsis‑induced cardiac dysfunction and pathogenetic mechanisms (Review).

Song J, Fang X, Zhou K, Bao H, Li L Mol Med Rep. 2023; 28(6).

PMID: 37859613 PMC: 10619129. DOI: 10.3892/mmr.2023.13114.


Diversity and complexity of cell death: a historical review.

Park W, Wei S, Kim B, Kim B, Bae S, Chae Y Exp Mol Med. 2023; 55(8):1573-1594.

PMID: 37612413 PMC: 10474147. DOI: 10.1038/s12276-023-01078-x.


References
1.
Tsai M, Jiang D, Zhao L, Clapham D, Miller C . Functional reconstitution of the mitochondrial Ca2+/H+ antiporter Letm1. J Gen Physiol. 2013; 143(1):67-73. PMC: 3874562. DOI: 10.1085/jgp.201311096. View

2.
Nowikovsky K, Pozzan T, Rizzuto R, Scorrano L, Bernardi P . Perspectives on: SGP symposium on mitochondrial physiology and medicine: the pathophysiology of LETM1. J Gen Physiol. 2012; 139(6):445-54. PMC: 3362517. DOI: 10.1085/jgp.201110757. View

3.
Crompton M, Kunzi M, Carafoli E . The calcium-induced and sodium-induced effluxes of calcium from heart mitochondria. Evidence for a sodium-calcium carrier. Eur J Biochem. 1977; 79(2):549-58. DOI: 10.1111/j.1432-1033.1977.tb11839.x. View

4.
Kirichok Y, Krapivinsky G, Clapham D . The mitochondrial calcium uniporter is a highly selective ion channel. Nature. 2004; 427(6972):360-4. DOI: 10.1038/nature02246. View

5.
Vasington F, Murphy J . Ca ion uptake by rat kidney mitochondria and its dependence on respiration and phosphorylation. J Biol Chem. 1962; 237:2670-7. View