Regulation of cytochrome c oxidase contributes to health and optimal life

Kadenbach, Bernhard

doi:10.4331/wjbc.v11.i2.52

Cited by 13 publications

(7 citation statements)

References 99 publications

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“…This step is also tightly regulated. Indeed, several regulatory mechanisms, including the allosteric regulation of COX and Cytc (e.g., by the ATP/ADP ratio) and reversible post-translational changes, including phosphorylation, were demonstrated [ 21 , 22 ].…”

Section: Mitochondria As Source Of Metabolic Energy Productionmentioning

confidence: 99%

Mitochondrial Management of Reactive Oxygen Species

Napolitano

Fasciolo²,

Venditti³

2021

Antioxidants

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Mitochondria in aerobic eukaryotic cells are both the site of energy production and the formation of harmful species, such as radicals and other reactive oxygen species, known as ROS. They contain an efficient antioxidant system, including low-molecular-mass molecules and enzymes that specialize in removing various types of ROS or repairing the oxidative damage of biological molecules. Under normal conditions, ROS production is low, and mitochondria, which are their primary target, are slightly damaged in a similar way to other cellular compartments, since the ROS released by the mitochondria into the cytosol are negligible. As the mitochondrial generation of ROS increases, they can deactivate components of the respiratory chain and enzymes of the Krebs cycle, and mitochondria release a high amount of ROS that damage cellular structures. More recently, the feature of the mitochondrial antioxidant system, which does not specifically deal with intramitochondrial ROS, was discovered. Indeed, the mitochondrial antioxidant system detoxifies exogenous ROS species at the expense of reducing the equivalents generated in mitochondria. Thus, mitochondria are also a sink of ROS. These observations highlight the importance of the mitochondrial antioxidant system, which should be considered in our understanding of ROS-regulated processes. These processes include cell signaling and the progression of metabolic and neurodegenerative disease.

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Section: Mitochondria As Source Of Metabolic Energy Productionmentioning

confidence: 99%

Mitochondrial Management of Reactive Oxygen Species

Napolitano

Fasciolo²,

Venditti³

2021

Antioxidants

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“…3 B). Although the reduction of complex IV is considered a ROS producing process [ 55 ], complex IV is a rate limiting step for the respiratory chain via an ATP-mediated allosteric inhibition [ 56 , 57 ]. Inhibition of ATP synthesis and simultaneously consumption of higher amounts of oxygen leads to ROS production in the mitochondria.…”

Section: Discussionmentioning

confidence: 99%

MnTE-2-PyP protects fibroblast mitochondria from hyperglycemia and radiation exposure

et al. 2022

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“…Speculatively, this allosteric effect may be behind the oscillation of [Ca 2+ ] m since each cycle of MCU-mediated Ca 2+ influx may transiently or locally decrease Δ Ψ m , whereas the concomitant fraction of imported Ca 2+ partially upregulates OXPHOS, hence adds to Δ Ψ m , which in turn would activate NCLX. The regulation of OXPHOS by cytosolic Ca 2+ penetrating into the ICS probably occurs via the Ca 2+ -induced activation of Complex IV subunit Cox4.1, which disrupts its feedback inhibition by ATP ( 39 , 114 , 203 ). The impact on GSIS is yet to be studied.…”

Section: Mitochondrial Ca 2+ Signaling In Pancreat...mentioning

confidence: 99%

Contribution of Mitochondria to Insulin Secretion by Various Secretagogues

Ježek

Holendová

Jabůrek

et al. 2022

Antioxidants & Redox Signaling

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Significance: Mitochondria determine glucose-stimulated insulin secretion (GSIS) in pancreatic b-cells by elevating ATP synthesis. As the metabolic and redox hub, mitochondria provide numerous links to the plasma membrane channels, insulin granule vesicles (IGVs), cell redox, NADH, NADPH, and Ca 2+ homeostasis, all affecting insulin secretion. Recent Advances: Mitochondrial redox signaling was implicated in several modes of insulin secretion (branched-chain ketoacid [BCKA]-, fatty acid [FA]-stimulated). Mitochondrial Ca 2+ influx was found to enhance GSIS, reflecting cytosolic Ca 2+ oscillations induced by action potential spikes (intermittent opening of voltage-dependent Ca 2+ and K + channels) or the superimposed Ca 2+ release from the endoplasmic reticulum (ER). The ATPase inhibitory factor 1 (IF1) was reported to tune the glucose sensitivity range for GSIS. Mitochondrial protein kinase A was implicated in preventing the IF1-mediated inhibition of the ATP synthase. Critical Issues: It is unknown how the redox signal spreads up to the plasma membrane and what its targets are, what the differences in metabolic, redox, NADH/NADPH, and Ca 2+ signaling, and homeostasis are between the first and second GSIS phase, and whether mitochondria can replace ER in the amplification of IGV exocytosis. Future Directions: Metabolomics studies performed to distinguish between the mitochondrial matrix and cytosolic metabolites will elucidate further details. Identifying the targets of cell signaling into mitochondria and of mitochondrial retrograde metabolic and redox signals to the cell will uncover further molecular mechanisms for insulin secretion stimulated by glucose, BCKAs, and FAs, and the amplification of secretion by glucagon-like peptide (GLP-1) and metabotropic receptors. They will identify the distinction between the hub b-cells and their followers in intact and diabetic states. Antioxid. Redox Signal. 00, 000-000.

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Regulation of cytochrome c oxidase contributes to health and optimal life

Cited by 13 publications

References 99 publications

Mitochondrial Management of Reactive Oxygen Species

Mitochondrial Management of Reactive Oxygen Species

MnTE-2-PyP protects fibroblast mitochondria from hyperglycemia and radiation exposure

Contribution of Mitochondria to Insulin Secretion by Various Secretagogues

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