Standing of giants shoulders the story of the mitochondrial Na+Ca2+ exchanger

Sekler, Israel

doi:10.1016/j.bbrc.2015.02.170

Cited by 20 publications

(11 citation statements)

References 27 publications

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“…Mitochondrial [Ca 2+ ] is regulated by the coordinated activity of influx and efflux pathways [101]. To assess the contribution of mitochondrial Ca 2+ efflux to heart pathophysiology, Elrod’s group recently developed an inducible mouse model with a cardiomyocyte-specific deletion of the Slc8b1 gene [55], which was previously demonstrated to encode the mitochondrial Na + /Ca 2+ exchanger (NCLX) [74].…”

Section: Mitochondrial Ca2+ Signaling In Physiology: General Framewormentioning

confidence: 99%

Mitochondrial calcium uptake in organ physiology: from molecular mechanism to animal models

Mammucari

Raffaello

Reane

et al. 2018

Pflugers Arch - Eur J Physiol

139

125

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Mitochondrial Ca2+ is involved in heterogeneous functions, ranging from the control of metabolism and ATP production to the regulation of cell death. In addition, mitochondrial Ca2+ uptake contributes to cytosolic [Ca2+] shaping thus impinging on specific Ca2+-dependent events. Mitochondrial Ca2+ concentration is controlled by influx and efflux pathways: the former controlled by the activity of the mitochondrial Ca2+ uniporter (MCU), the latter by the Na+/Ca2+ exchanger (NCLX) and the H+/Ca2+ (mHCX) exchanger. The molecular identities of MCU and of NCLX have been recently unraveled, thus allowing genetic studies on their physiopathological relevance. After a general framework on the significance of mitochondrial Ca2+ uptake, this review discusses the structure of the MCU complex and the regulation of its activity, the importance of mitochondrial Ca2+ signaling in different physiological settings, and the consequences of MCU modulation on organ physiology.

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Section: Mitochondrial Ca2+ Signaling In Physiology: General Framewormentioning

confidence: 99%

Mitochondrial calcium uptake in organ physiology: from molecular mechanism to animal models

Mammucari

Raffaello

Reane

et al. 2018

Pflugers Arch - Eur J Physiol

139

125

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“…Regulatory function of ions can be mediated either through direct binding to “sensor” proteins or indirectly through modulation of ion-dependent plasmalemmal transporters. Molecular physiology of Ca 2+ signalling has been extensively studied (Berridge et al , 2000; Burdakov et al , 2005; Petersen et al , 2005; Verkhratsky, 2005; Clapham, 2007; Petersen & Verkhratsky, 2007; Sekler, 2015), intracellular fluctuations of Na + have been shown to affect multiple membrane exchangers and trigger enzymatic and translational responses (Kirischuk et al , 2012), cytoplasmic K + regulates protein synthesis, whereas cytoplasmic Cl − may affect phosphorylation-associated signalling cascades ((Orlov & Hamet, 2006)).…”

Section: Principles Of Ionic Signallingmentioning

confidence: 99%

Crosslink between calcium and sodium signalling

Verkhratsky

Trebak

Perocchi

et al. 2018

Experimental Physiology

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Transmembrane ionic gradients, which are an indispensable feature of life, are used for generation of cytosolic ionic signals that regulate a host of cellular functions. Intracellular signalling mediated by Ca and Na is tightly linked through several molecular pathways that generate Ca and Na fluxes and are in turn regulated by both ions. Transient receptor potential (TRP) channels bridge endoplasmic reticulum Ca release with generation of Na and Ca currents. The plasmalemmal Na -Ca exchanger (NCX) flickers between forward and reverse mode to co-ordinate the influx and efflux of both ions with membrane polarization and cytosolic ion concentrations. The mitochondrial calcium uniporter channel (MCU) and mitochondrial Na -Ca exchanger (NCLX) mediate Ca entry into and release from this organelle and couple cytosolic Ca and Na fluctuations with cellular energetics. Cellular Ca and Na signalling controls numerous functional responses and, in the CNS, provides for fast regulation of astroglial homeostatic cascades that are crucial for maintenance of synaptic transmission.

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“…Slc8b1 encodes the mitochondrial Na + /Ca 2+ exchanger (NCLX), which is proposed to be the primary mechanism for m Ca 2+ extrusion in excitable cells 2,3 . Here we show that tamoxifen-induced deletion of Slc8b1 in adult mouse hearts causes sudden death, with less than 13% of affected mice surviving after 14 days.…”

mentioning

confidence: 99%

The mitochondrial Na+/Ca2+ exchanger is essential for Ca2+ homeostasis and viability

Luongo

Lambert

Gross

et al. 2017

Nature

331

284

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Mitochondrial calcium ( m Ca 2+ ) has a central role in both metabolic regulation and cell death signalling, however its role in homeostatic function and disease is controversial 1 . Slc8b1 encodes the mitochondrial Na + /Ca 2+ exchanger (NCLX), which is proposed to be the primary mechanism for m Ca 2+ extrusion in excitable cells 2,3 . Here we show that tamoxifen-induced deletion of Slc8b1Reprints and permissions information is available at www.nature.com/reprints.

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Standing of giants shoulders the story of the mitochondrial Na+Ca2+ exchanger

Cited by 20 publications

References 27 publications

Mitochondrial calcium uptake in organ physiology: from molecular mechanism to animal models

Mitochondrial calcium uptake in organ physiology: from molecular mechanism to animal models

Crosslink between calcium and sodium signalling

The mitochondrial Na+/Ca2+ exchanger is essential for Ca2+ homeostasis and viability

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