Cell energy metabolism: An update

Rigoulet, Michel; Bouchez, Cyrielle L.; Paumard, Patrick; Ransac, Stéphane; Cuvellier, Sylvain; Duvezin-Caubet, Stéphane; Mazat, Jean‐Pierre; Devin, Anne

doi:10.1016/j.bbabio.2020.148276

Cited by 88 publications

(59 citation statements)

References 120 publications

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“…Cell growth and survival depend on constant ATP regeneration in order to sustain motor proteins (e.g., muscle contraction, vesicle trafficking), ion pumping, protoplasmic streaming, cytoskeletal rearrangement, among others. ATP is synthesized either through substrate-level phosphorylation or through oxidative phosphorylation [83]; however, to guarantee it is mostly used in contraction machinery, ATPase pumps, and other organelles (i.e., nucleus, endoplasmic reticulum, etc. ), the cell relies on a phosphotransfer network that is based on the CK/PCr system [84].…”

Section: How Is the Ck/pcr System Involved In Cellular Bioenergetics?mentioning

confidence: 99%

Metabolic Basis of Creatine in Health and Disease: A Bioinformatics-Assisted Review

et al. 2021

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Creatine (Cr) is a ubiquitous molecule that is synthesized mainly in the liver, kidneys, and pancreas. Most of the Cr pool is found in tissues with high-energy demands. Cr enters target cells through a specific symporter called Na+/Cl−-dependent Cr transporter (CRT). Once within cells, creatine kinase (CK) catalyzes the reversible transphosphorylation reaction between [Mg2+:ATP4−]2− and Cr to produce phosphocreatine (PCr) and [Mg2+:ADP3−]−. We aimed to perform a comprehensive and bioinformatics-assisted review of the most recent research findings regarding Cr metabolism. Specifically, several public databases, repositories, and bioinformatics tools were utilized for this endeavor. Topics of biological complexity ranging from structural biology to cellular dynamics were addressed herein. In this sense, we sought to address certain pre-specified questions including: (i) What happens when creatine is transported into cells? (ii) How is the CK/PCr system involved in cellular bioenergetics? (iii) How is the CK/PCr system compartmentalized throughout the cell? (iv) What is the role of creatine amongst different tissues? and (v) What is the basis of creatine transport? Under the cellular allostasis paradigm, the CK/PCr system is physiologically essential for life (cell survival, growth, proliferation, differentiation, and migration/motility) by providing an evolutionary advantage for rapid, local, and temporal support of energy- and mechanical-dependent processes. Thus, we suggest the CK/PCr system acts as a dynamic biosensor based on chemo-mechanical energy transduction, which might explain why dysregulation in Cr metabolism contributes to a wide range of diseases besides the mitigating effect that Cr supplementation may have in some of these disease states.

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Section: How Is the Ck/pcr System Involved In Cellular Bioenergetics?mentioning

confidence: 99%

Metabolic Basis of Creatine in Health and Disease: A Bioinformatics-Assisted Review

et al. 2021

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“…The conversion of glucose and oxygen to ATP, CO2, and water takes place by glycolysis, the TCA cycle, and the ETC [89]. Glycolysis is a ten-step cytosolic pathway that converts glucose into pyruvate, ADP to ATP, and nicotinamide adenine dinucleotide (NAD + ) to reduced nicotinamide adenine dinucleotide (NADH) [90][91][92]. Pyruvate is oxidized and utilized in the TCA cycle, a series of chemical reactions in the mitochondrial matrix that release energy from acetyl-CoA [90][91][92].…”

Section: Zinc and Bioenergetic Functionmentioning

confidence: 99%

“…Glycolysis is a ten-step cytosolic pathway that converts glucose into pyruvate, ADP to ATP, and nicotinamide adenine dinucleotide (NAD + ) to reduced nicotinamide adenine dinucleotide (NADH) [90][91][92]. Pyruvate is oxidized and utilized in the TCA cycle, a series of chemical reactions in the mitochondrial matrix that release energy from acetyl-CoA [90][91][92]. This released energy is stored in electron carriers NADH and flavin adenine dinucleotide (FADH2), which are utilized by complexes of the ETC [90][91][92].…”

Section: Zinc and Bioenergetic Functionmentioning

confidence: 99%

“…Pyruvate is oxidized and utilized in the TCA cycle, a series of chemical reactions in the mitochondrial matrix that release energy from acetyl-CoA [90][91][92]. This released energy is stored in electron carriers NADH and flavin adenine dinucleotide (FADH2), which are utilized by complexes of the ETC [90][91][92]. NADH donates its electrons to complex I and FADH2 donates its electrons to complex II, and these electrons are transferred in succession to ubiquinone (coenzyme Q), complex III, the mobile electron carrier cytochrome C, complex IV, and the final electron acceptor, oxygen [93].…”

Section: Zinc and Bioenergetic Functionmentioning

confidence: 99%

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The Multifaceted Roles of Zinc in Neuronal Mitochondrial Dysfunction

Liu

Gale

Reynolds³

et al. 2021

Preprint

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Zinc is a highly abundant cation in the brain, where it is essential for cellular function, including transcription, enzymatic activity, and cell signaling. However, zinc can also trigger injurious cascades in neurons, contributing to the pathology of neurodegenerative diseases. Mitochondria, critical for meeting the high energy demands of the central nervous system (CNS), are a principal target of the deleterious actions of zinc. An increasing body of work suggests that intracellular zinc, can, under certain circumstances, contribute to neuronal damage by inhibiting mitochondrial energy processes, including dissipation of the mitochondrial membrane potential, leading to ATP depletion. Additional consequences of zinc-mediated mitochondrial damage include reactive oxygen species (ROS) generation, mitochondrial permeability transition, and calcium deregulation. Zinc can also induce mitochondrial fission, resulting in mitochondrial fragmentation, as well as inhibition of mitochondrial motility. Here, we review the known mechanisms responsible for the deleterious actions of zinc on the organelle, within the context of neuronal injury associated with neurodegenerative processes. Elucidating the critical contributions of zinc-induced mitochondrial defects to neurotoxicity and neurodegeneration may provide insight into novel therapeutic targets in the clinical setting.

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“…Glycolysis and oxidative phosphorylation (OXPHOS) are the major energy providers to cells [1,2]. In aerobic cells, the vast majority of chemical energy is produced by the mitochondria as ATP.…”

Section: Introductionmentioning

confidence: 99%

Cells Lacking PA200 Adapt to Mitochondrial Dysfunction by Enhancing Glycolysis via Distinct Opa1 Processing

Douida

Batista

Botó

et al. 2021

IJMS

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The conserved Blm10/PA200 proteins are proteasome activators. Previously, we identified PA200-enriched regions in the genome of SH-SY5Y neuroblastoma cells by chromatin immunoprecipitation (ChIP) and ChIP-seq analysis. We also found that selective mitochondrial inhibitors induced PA200 redistribution in the genome. Collectively, our data indicated that PA200 regulates cellular homeostasis at the transcriptional level. In the present study, our aim is to investigate the impact of stable PA200 depletion (shPA200) on the overall transcriptome of SH-SY5Y cells. RNA-seq data analysis reveals that the genetic ablation of PA200 leads to overall changes in the transcriptional landscape of SH-SY5Y neuroblastoma cells. PA200 activates and represses genes regulating metabolic processes, such as the glycolysis and mitochondrial function. Using metabolic assays in live cells, we showed that stable knockdown of PA200 does not change basal respiration. Spare respiratory capacity and proton leak however are slightly, yet significantly, reduced in PA200-deficient cells by 99.834% and 84.147%, respectively, compared to control. Glycolysis and glycolytic capacity show a 42.186% and 26.104% increase in shPA200 cells, respectively, compared to control. These data suggest a shift from oxidative phosphorylation to glycolysis especially when cells are exposed to oligomycin-induced stress. Furthermore, we observed a preserved long and compact tubular mitochondrial morphology after inhibition of ATP synthase by oligomycin, which might be associated with the glycolytic change of shPA200 cells. The present study also demonstrates that the proteolytic cleavage of Opa1 is affected, and that the level of OMA1 is significantly reduced in shPA200 cells upon oligomycin-induced mitochondrial insult. Together, these findings suggest a role for PA200 in the regulation of metabolic changes in response to selective inhibition of ATP synthase in an in vitro cellular model.

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Cell energy metabolism: An update

Cited by 88 publications

References 120 publications

Metabolic Basis of Creatine in Health and Disease: A Bioinformatics-Assisted Review

Metabolic Basis of Creatine in Health and Disease: A Bioinformatics-Assisted Review

The Multifaceted Roles of Zinc in Neuronal Mitochondrial Dysfunction

Cells Lacking PA200 Adapt to Mitochondrial Dysfunction by Enhancing Glycolysis via Distinct Opa1 Processing

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