Mitochondrial Calcium Signalling: Role in Oxidative Phosphorylation Diseases

Oulès, Bénédicte; Dolores, Del Prete; Chami, Mounia

doi:10.5772/32117

Cited by 3 publications

(5 citation statements)

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“…120,121 The main mechanism of ER calcium release is through inositol-1,4,5-trisphosphate (IP3), which activates the IP3 receptor (IP3 R) on the ER membrane, leading to Ca +2 release into the cytosol. 122,123 The cAMP/PKA pathway plays an important role in Ca + signaling, with PKA modulating both IP3 R capacity 124 and NMDAR permeability for extracellular Ca +2 . 30 Cytosolic Ca +2 enters the mitochondria via the Ca +2 uniporter, due to the membrane potential driving force generated by the OXPHOS.…”

Section: The Oxphos and Calcium Homeostasismentioning

confidence: 99%

“…30 Cytosolic Ca +2 enters the mitochondria via the Ca +2 uniporter, due to the membrane potential driving force generated by the OXPHOS. 123,125 Intramitochondrial Ca +2 ( Ca im +2 ) affects OXPHOS function through different mechanisms. For example, Ca im +2 modulates and stimulates sAC activity and thereby the PKA signaling cascade.…”

Section: The Oxphos and Calcium Homeostasismentioning

confidence: 99%

“…127,128 Ca im +2 has been suggested to facilitate activation, regulation, and proper function of OXPHOS genes by activating key dehydrogenases of citric acid, including pyruvate dehydrogenase, NAD + -isocitrate dehydrogenase, and oxoglutarate dehydrogenase. 123,129,130 A direct effect of Ca im +2 on regulation of ATP production has been suggested via the activation of complex V and an increase of electron flow through CoIII. 131,132 A reciprocal interaction between OXPHOS and Ca im +2 has been suggested as CoI, CoII, and CoIV deficiencies are associated with abnormalities in Ca +2 signaling.…”

Section: The Oxphos and Calcium Homeostasismentioning

confidence: 99%

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Mitochondrial Oxidative Phosphorylation System (OXPHOS) Deficits in Schizophrenia

2016

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Mitochondria are key players in the generation and regulation of cellular bioenergetics, producing the majority of adenosine triphosphate molecules by the oxidative phosphorylation system (OXPHOS). Linked to numerous signaling pathways and cellular functions, mitochondria, and OXPHOS in particular, are involved in neuronal development, connectivity, plasticity, and differentiation. Impairments in a variety of mitochondrial functions have been described in different general and psychiatric disorders, including schizophrenia (SCZ), a severe, chronic, debilitating illness that heavily affects the lives of patients and their families. This article reviews findings emphasizing the role of OXPHOS in the pathophysiology of SCZ. Evidence accumulated during the past few decades from imaging, transcriptomic, proteomic, and metabolomic studies points at OXPHOS deficit involvement in SCZ. Abnormalities have been reported in high-energy phosphates generated by the OXPHOS, in the activity of its complexes and gene expression, primarily of complex I (CoI). In addition, cellular signaling such as cAMP/protein kinase A (PKA) and Ca þ2 , neuronal development, connectivity, and plasticity have been linked to OXPHOS function and are reported to be impaired in SCZ. Finally, CoI has been shown as a site of interaction for both dopamine (DA) and antipsychotic drugs, further substantiating its role in the pathology of SCZ. Understanding the role of mitochondria and the OXPHOS in particular may encourage new insights into the pathophysiology and etiology of this debilitating disorder. Abré géLes mitochondries sont un acteur clé dans la génération et la régulation de la bioénergétique cellulaire, produisant la majorité des molécules ATP par le système de phosphorylation oxydative (OXPHOS). Liées à de nombreuses voies de signalisation et fonctions cellulaires, les mitochondries, et OXPHOS en particulier, sont impliqués dans le développement neuronal, la connectivité, la plasticité et la différenciation. Des déficiences d'une variété de fonctions mitochondriales ont été décrites dans différents troubles généraux et psychiatriques, dont la schizophrénie (SCZ), une maladie grave, chronique et débilitante qui affecte lourdement la vie des patients et de leur famille. Cet article passe en revue les résultats mettant l'accent sur le rô le d'OXPHOS dans la pathophysiologie de la SCZ. Les données probantes accumulées au cours des récentes décennies dans des études d'imagerie, transcriptomiques, protéomiques et métabolomiques dénoncent la participation du déficit d'OXPHOS à la SCZ. Des anomalies ont été signalées dans les phosphates à haute énergie produits par le système OXPHOS, dans l'activité de ses complexes et de son expression génétique, principalement du complexe I (CoI). En outre, la signalisation cellulaire, comme

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Section: The Oxphos and Calcium Homeostasismentioning

confidence: 99%

Section: The Oxphos and Calcium Homeostasismentioning

confidence: 99%

Section: The Oxphos and Calcium Homeostasismentioning

confidence: 99%

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Mitochondrial Oxidative Phosphorylation System (OXPHOS) Deficits in Schizophrenia

2016

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“…With respect to the latter topic, the present model becomes particularly relevant during actuation of intracellular compartmental Ca 2+ loading from interstitial and intracellular cation sources. Even as a preliminary construct, the model implies contexts coincident with moderate to massive fluxes of Ca 2+ through cation-permeable integral cell membrane pores and gated channels, such as during synaptic plasticity (Malenka and Bear, 2004 ), microbial pathogen attack (Clark, 2013b ; Clark and Eisenstein, 2013 ; Clark et al, 2013 ), pathological oxidative stress (Bénédicte et al, 2012 ; Clark, 2012c ), and neurological disease and aging (Verkhratsky, 2005 ; Bezprozvanny and Mattson, 2008 ; Stutzmann and Mattson, 2011 ), will assist in driving neurons to accelerate response regulation to quantum-level efficiency through induction of stable local and possibly subsequent global continuous Ca 2+ waves. From a physiological perspective, dramatic increases in Ca 2+ wave velocity and signal transduction at either intracluster or intercluster physical dimensions are impressive and attainable for a all sorts of differentiated eukaryotic cells (cf.…”

Section: Relevance Of Grover's Quantum Algorithm For Healthy and Disementioning

confidence: 99%

Basis for a neuronal version of Grover's quantum algorithm

Clark

2014

Front. Mol. Neurosci.

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Grover's quantum (search) algorithm exploits principles of quantum information theory and computation to surpass the strong Church–Turing limit governing classical computers. The algorithm initializes a search field into superposed N (eigen)states to later execute nonclassical “subroutines” involving unitary phase shifts of measured states and to produce root-rate or quadratic gain in the algorithmic time (O(N1/2)) needed to find some “target” solution m. Akin to this fast technological search algorithm, single eukaryotic cells, such as differentiated neurons, perform natural quadratic speed-up in the search for appropriate store-operated Ca2+ response regulation of, among other processes, protein and lipid biosynthesis, cell energetics, stress responses, cell fate and death, synaptic plasticity, and immunoprotection. Such speed-up in cellular decision making results from spatiotemporal dynamics of networked intracellular Ca2+-induced Ca2+ release and the search (or signaling) velocity of Ca2+ wave propagation. As chemical processes, such as the duration of Ca2+ mobilization, become rate-limiting over interstore distances, Ca2+ waves quadratically decrease interstore-travel time from slow saltatory to fast continuous gradients proportional to the square-root of the classical Ca2+ diffusion coefficient, D1/2, matching the computing efficiency of Grover's quantum algorithm. In this Hypothesis and Theory article, I elaborate on these traits using a fire-diffuse-fire model of store-operated cytosolic Ca2+ signaling valid for glutamatergic neurons. Salient model features corresponding to Grover's quantum algorithm are parameterized to meet requirements for the Oracle Hadamard transform and Grover's iteration. A neuronal version of Grover's quantum algorithm figures to benefit signal coincidence detection and integration, bidirectional synaptic plasticity, and other vital cell functions by rapidly selecting, ordering, and/or counting optional response regulation choices.

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“…In autism, low plasma Ca 2+ and high brain Ca 2+ readily leads to oxidative stress as mitochondrial oxygen radical is stimulated by increased intracellular Ca 2+17, 18. Calcium plays an important role in the activation of different essential enzymes in energy producing pathways, such as á-ketoglutarate dehydrogenase, isocitrate dehydrogenase and pyruvate dehydrogenase 19,20 .…”

Section: Introductionmentioning

confidence: 99%

Study On Serum Magnesium, Calcium And Iron In Autism Spectrum Disorder (ASD) Children

Shahjadi¹,

Khan²,

Ahmed³

et al. 2020

J Dhaka Med Coll

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Background: Autism is a complex neurodevelopmental disorder and one of the major cause of lifelong disability. Magnesium, calcium and iron are important minerals of biological system. Hypomagnesaemia, hypocalcaemia and iron deficiency has been found to be associated with abnormal metabolic functions resulting in autistic spectrum disorder. Hypothesis: Serum magnesium, calcium and iron levels are lower in ASD children than healthy control. Objective: To measure serum magnesium, calcium and iron in ASDchildren and to compare them with healthy control. Method: This observational type of analytical study with case-control design was conducted in the Department of Physiology, Bangabandhu Sheikh Mujib Medical University, Shahbag, Dhaka from March 2014–January 2016. For this study, 80 children aged 3-10 years were randomly selected, among which 40 were apparently healthy and 40 were diagnosed as ASD. The study group was selected from the Parents’ Forum (Mohakhali DOHS, Dhaka) for ASD children and the control group was selected from some regular schools. 5ml venous blood was collected from both groups for analysis of fasting serum magnesium, calcium and iron. Fasting magnesium, calcium and iron were estimated in all children by standard laboratory method. Independent sample‘t’ test and proportion (Z) test were used for statistical analysis. P value Â0.05 was accepted as significant. Result: The mean serum magnesium, calcium and iron were significantly lower (pÂ0.001) in cases as compared to controls. The frequency of hypomagnesaemia, hypocalcaemia and iron deficiency were significantly higher in early diagnosed ASD children, which was 7 (17.5%), 22 (55%) and 5 (12.5%) out of 40 ASD children respectively.The mean values of all the biochemical variables in normal children were within normal ranges. Conclusion: The results indicate that hypomagnesaemia, hypocalcaemia and iron deficiency are common in ASD children. J Dhaka Medical College, Vol. 27, No.2, October, 2018, Page 199-204

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Mitochondrial Calcium Signalling: Role in Oxidative Phosphorylation Diseases

Cited by 3 publications

References 168 publications

Mitochondrial Oxidative Phosphorylation System (OXPHOS) Deficits in Schizophrenia

Mitochondrial Oxidative Phosphorylation System (OXPHOS) Deficits in Schizophrenia

Basis for a neuronal version of Grover's quantum algorithm

Study On Serum Magnesium, Calcium And Iron In Autism Spectrum Disorder (ASD) Children

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