Mitochondrial Ca2+ Transport: Mechanisms, Molecular Structures, and Role in Cells

Belosludtsev, Konstantin N.; Dubinin, Mikhail V.; Belosludtseva, Natalia V.; Mironova, Galina D.

doi:10.1134/s0006297919060026

Cited by 118 publications

(130 citation statements)

References 108 publications

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“…It is known that the activity of MCUC is regulated by changes in the ratio of the Ca 2+ -conducting pore subunits MCU and MCUb [5,26,27]. Therefore, both an increase in the level of MCU and a decrease in the content of its paralogue MCUb, which we recorded in mitochondria of the liver and heart of HR animals, can be the cause of the increased rate of Ca 2+ influx into the organelles.…”

Section: Discussionmentioning

confidence: 59%

“…As for heart tissue, a comparative analysis of the protein level of the components of the MCUC showed that there was a significant decrease in the content of MCUb and a slight tendency to an increase in the content of MCU in the cardiac mitochondria of HR rats relative to those of LR animals ( Figure 2C,D). VDAC1 participates in the formation of MAM (mitochondria-associated membranes) contacts, which are the main pathway of Ca 2+ transfer from the endoplasmic reticulum to mitochondria [5,14]. One can see that the amount of VDAC1 in liver mitochondria did not differ.…”

Section: Mitochondrial Ca 2+ Uptake and The Features Of Subunit Compomentioning

confidence: 89%

“…It is believed that VDAC1 is also involved in the formation of the MPT pore complex in mitochondria. In addition, this protein participates in the formation of MAM contacts, which are the main pathway of Ca 2+ transfer from the endoplasmic reticulum to mitochondria [5,14]. So, the changes observed in the level of VDAC1 can also contribute to the tissue-specific modulation of mitochondrial Ca 2+ handling and the MTP opening.…”

Section: Discussionmentioning

confidence: 99%

“…Mitochondrial Ca 2+ uptake is mediated by an electrogenic uniport, referred to as "Ca 2+ uniporter", a complex of proteins of the inner mitochondrial membrane, including the pore-forming subunit MCU and its dominant-negative form MCUb, and the regulatory subunits MICU1, MICU2, EMRE, and MCUR1. It is considered that the contents of MCU, MCUb, and MICU1 and their stoichiometry can predominantly regulate the mitochondrial Ca 2+ transport in accordance with physiological needs [5,6,23]. Since the mitochondria of HR animals accumulate Ca 2+ faster as compared to the organelles of LR rats, one can assume that the adaptation to hypoxic stress is associated with changes in the relative content of these subunits in the mitochondrial membrane.…”

Section: Mitochondrial Ca 2+ Uptake and The Features Of Subunit Compomentioning

confidence: 99%

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Transport of Ca2+ and Ca2+-Dependent Permeability Transition in the Liver and Heart Mitochondria of Rats with Different Tolerance to Acute Hypoxia

et al. 2020

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The work examines the kinetic parameters of Ca2+ uptake via the mitochondrial calcium uniporter complex (MCUC) and the opening of the Ca2+-dependent permeability transition pore (MPT pore) in the liver and heart mitochondria of rats with high resistance (HR) and low resistance (LR) to acute hypoxia. We found that the rate of Ca2+ uptake by mitochondria of the liver and heart in HR rats is higher than that in LR rats, which is associated with a higher level of the channel-forming subunit MCU in liver mitochondria of HR rats and a lower content of the dominant-negative channel subunit MCUb in heart mitochondria of HR rats. It was shown that the liver mitochondria of HR rats are more resistant to the induction of the MPT pore than those of LR rats (the calcium retention capacity of liver mitochondria of HR rats was found to be 1.3 times greater than that of LR rats). These data correlate with the fact that the level of F0F1-ATP synthase, a possible structural element of the MPT pore, in the liver mitochondria of HR rats is lower than in LR rats. In heart mitochondria of rats of the two phenotypes, no statistically significant difference in the formation of the MPT pore was revealed. The paper discusses how changes in the expression of the MCUC subunits and the putative components of the MPT pore can affect Ca2+ homeostasis of mitochondria in animals with originally different tolerance to hypoxia and in hypoxia-induced tissue injury.

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Section: Discussionmentioning

confidence: 59%

Section: Mitochondrial Ca 2+ Uptake and The Features Of Subunit Compomentioning

confidence: 89%

Section: Discussionmentioning

confidence: 99%

Section: Mitochondrial Ca 2+ Uptake and The Features Of Subunit Compomentioning

confidence: 99%

See 2 more Smart Citations

Transport of Ca2+ and Ca2+-Dependent Permeability Transition in the Liver and Heart Mitochondria of Rats with Different Tolerance to Acute Hypoxia

et al. 2020

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“…Regulation of free intracellular concentration of Ca 2+ is an important mechanism for intracellular signaling, and it is a key component in the mediation of many cell functions and biochemical reactions, being crucial for signal transduction in cells [ 2 , 6 , 7 , 8 , 9 , 10 ]. On top of all that, intra-mitochondrial Ca 2+ regulates a cascade of physiological and pathophysiological processes in cells [ 10 , 11 , 12 , 13 , 14 , 15 ].…”

Section: Introductionmentioning

confidence: 99%

Regulation of Cell Death by Mitochondrial Transport Systems of Calcium and Bcl-2 Proteins

Naumova

Šachl

2020

Membranes

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Mitochondria represent the fundamental system for cellular energy metabolism, by not only supplying energy in the form of ATP, but also by affecting physiology and cell death via the regulation of calcium homeostasis and the activity of Bcl-2 proteins. A lot of research has recently been devoted to understanding the interplay between Bcl-2 proteins, the regulation of these interactions within the cell, and how these interactions lead to the changes in calcium homeostasis. However, the role of Bcl-2 proteins in the mediation of mitochondrial calcium homeostasis, and therefore the induction of cell death pathways, remain underestimated and are still not well understood. In this review, we first summarize our knowledge about calcium transport systems in mitochondria, which, when miss-regulated, can induce necrosis. We continue by reviewing and analyzing the functions of Bcl-2 proteins in apoptosis. Finally, we link these two regulatory mechanisms together, exploring the interactions between the mitochondrial Ca2+ transport systems and Bcl-2 proteins, both capable of inducing cell death, with the potential to determine the cell death pathway—either the apoptotic or the necrotic one.

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Structural and Functional Features of Ca2+ Transport Systems in Liver Mitochondria of Rats with Experimental Hyperthyroidism

et al. 2020

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Mitochondrial Ca2+ Transport: Mechanisms, Molecular Structures, and Role in Cells

Cited by 118 publications

References 108 publications

Transport of Ca2+ and Ca2+-Dependent Permeability Transition in the Liver and Heart Mitochondria of Rats with Different Tolerance to Acute Hypoxia

Transport of Ca2+ and Ca2+-Dependent Permeability Transition in the Liver and Heart Mitochondria of Rats with Different Tolerance to Acute Hypoxia

Regulation of Cell Death by Mitochondrial Transport Systems of Calcium and Bcl-2 Proteins

Structural and Functional Features of Ca2+ Transport Systems in Liver Mitochondria of Rats with Experimental Hyperthyroidism

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