A crosstalk between Na+ channels, Na+/K+ pump and mitochondrial Na+ transporters controls glucose-dependent cytosolic and mitochondrial Na+ signals

Nita, Iulia I.; Hershfinkel, Michal; Lewis, Eli C.; Sekler, Israel

doi:10.1016/j.ceca.2014.12.007

Cited by 27 publications

(16 citation statements)

References 32 publications

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“…Unlike NCLX, the NCX effect on cytosolic Ca 2+ is not mediated through direct action on CRAC conductance. Therefore, our current and previous studies (Borin et al , ; Lemos et al , ; Nita et al , ,b) indicate that NCLX and NCX concertedly amplify SOCE‐dependent cytosolic Ca 2+ signals but through different mechanisms. For NCX, the SOCE‐dependent Na + rise triggers its reverse mode leading to increased cytosolic Ca 2+ while for NCLX it triggers forward activation that can lead to maintenance of CRAC channel activity (Fig ).…”

Section: Discussionsupporting

confidence: 57%

Mitochondria control store‐operated Ca ²⁺ entry through Na ⁺ and redox signals

et al. 2017

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Section: Discussionsupporting

confidence: 57%

Mitochondria control store‐operated Ca ²⁺ entry through Na ⁺ and redox signals

et al. 2017

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“…The discovery of the molecular identity of mNCLX (Palty et al 2010) was instrumental for understanding the molecular mechanisms of mitochondrial Ca 2+ homeostasis. Accordingly, a functional crosstalk between mNCLX and other Na + and Ca 2+ transporters located on both mitochondrial and plasma membranes has been described (Nita et al 2015;Ben-Kasus Nissim et al 2017), underscoring the significant physiological role of mNCLX for the regulation of both Ca 2+ and Na + signalling pathways.…”

Section: Mitochondrial Ca 2+ Effluxmentioning

confidence: 99%

“…Accordingly, a functional crosstalk between mNCLX and other Na + and Ca 2+ transporters located on both mitochondrial and plasma membranes has been described (Nita et al . ; Ben‐Kasus Nissim et al . ), underscoring the significant physiological role of mNCLX for the regulation of both Ca 2+ and Na + signalling pathways.…”

Section: Introductionmentioning

confidence: 99%

Pharmacological modulation of mitochondrial calcium homeostasis

Arduíno

Perocchi

2018

The Journal of Physiology

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Mitochondria are pivotal organelles in calcium (Ca ) handling and signalling, constituting intracellular checkpoints for numerous processes that are vital for cell life. Alterations in mitochondrial Ca homeostasis have been linked to a variety of pathological conditions and are critical in the aetiology of several human diseases. Efforts have been taken to harness mitochondrial Ca transport mechanisms for therapeutic intervention, but pharmacological compounds that direct and selectively modulate mitochondrial Ca homeostasis are currently lacking. New avenues have, however, emerged with the breakthrough discoveries on the genetic identification of the main players involved in mitochondrial Ca influx and efflux pathways and with recent hints towards a deep understanding of the function of these molecular systems. Here, we review the current advances in the understanding of the mechanisms and regulation of mitochondrial Ca homeostasis and its contribution to physiology and human disease. We also introduce and comment on the recent progress towards a systems-level pharmacological targeting of mitochondrial Ca homeostasis.

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“…; Nita et al . ). Thus, elevated [Na + ] CYT and/or [Ca 2+ ] CYT (which should limit NCLX‐mediated Ca 2+ export) can not only enhance Ca 2+ signalling, but also increase oxidative stress and ROS production (Li et al .…”

Section: Introductionmentioning

confidence: 97%

Pivotal role of α2 Na⁺ pumps and their high affinity ouabain binding site in cardiovascular health and disease

Blaustein

Chen

Hamlyn

et al. 2016

The Journal of Physiology

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Reduced smooth muscle (SM)-specific α2 Na pump expression elevates basal blood pressure (BP) and increases BP sensitivity to angiotensin II (Ang II) and dietary NaCl, whilst SM-α2 overexpression lowers basal BP and decreases Ang II/salt sensitivity. Prolonged ouabain infusion induces hypertension in rodents, and ouabain-resistant mutation of the α2 ouabain binding site (α2 mice) confers resistance to several forms of hypertension. Pressure overload-induced heart hypertrophy and failure are attenuated in cardio-specific α2 knockout, cardio-specific α2 overexpression and α2 mice. We propose a unifying hypothesis that reconciles these apparently disparate findings: brain mechanisms, activated by Ang II and high NaCl, regulate sympathetic drive and a novel neurohumoral pathway mediated by both brain and circulating endogenous ouabain (EO). Circulating EO modulates ouabain-sensitive α2 Na pump activity and Ca transporter expression and, via Na /Ca exchange, Ca homeostasis. This regulates sensitivity to sympathetic activity, Ca signalling and arterial and cardiac contraction.

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A crosstalk between Na+ channels, Na+/K+ pump and mitochondrial Na+ transporters controls glucose-dependent cytosolic and mitochondrial Na+ signals

Cited by 27 publications

References 32 publications

Mitochondria control store‐operated Ca ²⁺ entry through Na ⁺ and redox signals

Mitochondria control store‐operated Ca ²⁺ entry through Na ⁺ and redox signals

Pharmacological modulation of mitochondrial calcium homeostasis

Pivotal role of α2 Na⁺ pumps and their high affinity ouabain binding site in cardiovascular health and disease

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A crosstalk between Na+ channels, Na+/K+ pump and mitochondrial Na+ transporters controls glucose-dependent cytosolic and mitochondrial Na+ signals

Cited by 27 publications

References 32 publications

Mitochondria control store‐operated Ca 2+ entry through Na + and redox signals

Mitochondria control store‐operated Ca 2+ entry through Na + and redox signals

Pharmacological modulation of mitochondrial calcium homeostasis

Pivotal role of α2 Na+ pumps and their high affinity ouabain binding site in cardiovascular health and disease

Contact Info

Product

Resources

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Mitochondria control store‐operated Ca ²⁺ entry through Na ⁺ and redox signals

Mitochondria control store‐operated Ca ²⁺ entry through Na ⁺ and redox signals

Pivotal role of α2 Na⁺ pumps and their high affinity ouabain binding site in cardiovascular health and disease