Correction: CAPER Is Vital for Energy and Redox Homeostasis by Integrating Glucose-Induced Mitochondrial Functions via ERR-α-Gabpa and Stress-Induced Adaptive Responses via NF-κB-cMYC

Our previous study in Goto-Kakizaki (GK) type 2 diabetic rats provided significant evidence that aspirin treatment improves pancreatic β-cell function by reducing inflammatory responses and improving glucose tolerance. In the present study, we aimed to elucidate the mechanism of action of aspirin on the pathophysiology and progression of type 2 diabetic complications in the heart and pancreas of insulin-resistant GK rats. Aspirin treatment demonstrated a reduction in mitochondrial reactive oxygen species (ROS) production and lipid peroxidation, accompanied by improved redox homeostasis. Furthermore, the recovery of metabolic and mitochondrial functions, as well as cytochrome P450 enzyme activities, which were altered in the pancreas and heart of GK rats, were observed. Aspirin treatment brought the activity of CYP 2E1 to the control level in both tissues, whereas the CYP 3A4 level decreased only in the pancreas. This suggests the tissue-specific differential metabolism of substrates in these rats. The recovery of redox homeostasis could be the key target in the improvement of oxidative-stress-dependent alterations in mitochondrial functions which, in turn, facilitated improved energy metabolism in these tissues in the aspirin-treated GK rats. These results may have implications in determining the therapeutic use of aspirin, either alone or in combination with other clinically approved therapies, in insulin-resistant type 2 diabetes.

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Crosstalk between mitochondrial metabolism and oxidoreductive homeostasis: a new perspective for understanding the effects of bioactive dietary compounds

Nutrition Research Reviews ◽

10.1017/s0954422419000210 ◽

2019 ◽

Vol 33 (1) ◽

pp. 90-101 ◽

Cited By ~ 1

Author(s):

Mariangela Di Giacomo ◽

Vincenzo Zara ◽

Paolo Bergamo ◽

Alessandra Ferramosca

Keyword(s):

Biological Effects ◽

Redox Homeostasis ◽

Natural Compounds ◽

Redox Status ◽

Mitochondrial Metabolism ◽

Functional Link ◽

Cellular Processes ◽

New Therapeutic Approaches ◽

Mitochondrial Functions ◽

New Perspective

AbstractMitochondria play an important role in a number of fundamental cellular processes, including energy production, biosynthetic pathways and cellular oxidoreductive homeostasis (redox status), and their dysfunction can lead to numerous pathophysiological consequences. As the biochemical mechanisms orchestrating mitochondrial metabolism and redox homeostasis are functionally linked, mitochondria have been identified as a potential therapeutic target. Consequently, considerable effort has been made to evaluate the efficacy of natural compounds that modulate mitochondrial function. Molecules produced by plants (for example, polyphenols and isothiocyanates) have been shown to modulate mitochondrial metabolism/biogenesis and redox status; however, despite the existence of a functional link, few studies have considered the combined efficacy of these mitochondrial functions. The present review provides a complete overview of the molecular pathways involved in modulating mitochondrial metabolism/biogenesis and redox status. Crosstalk between these critical mechanisms is also discussed, whilst major data from the literature regarding their antioxidant abilities are described and critically analysed. We also provide a summary of recent evidence regarding the ability of several plant-derived compounds to target these mitochondrial functions. An in-depth understanding of the functional link between mitochondrial metabolism/biogenesis and redox status could facilitate the analysis of the biological effects of natural compounds as well as the development of new therapeutic approaches.

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Vitamin E-enriched diet reduces adaptive responses to training determining respiratory capacity and redox homeostasis in rat heart

Free Radical Research ◽

10.3109/10715762.2015.1106530 ◽

2015 ◽

Vol 50 (1) ◽

pp. 56-67 ◽

Cited By ~ 4

Author(s):

Paola Venditti ◽

Gaetana Napolitano ◽

Daniela Barone ◽

Emanuela Pervito ◽

Sergio Di Meo

Keyword(s):

Vitamin E ◽

Rat Heart ◽

Redox Homeostasis ◽

Adaptive Responses ◽

Respiratory Capacity

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The contralateral kidney presents with impaired mitochondrial functions and disrupted redox homeostasis after 14 days of unilateral ureteral obstruction in mice

PLoS ONE ◽

10.1371/journal.pone.0218986 ◽

2019 ◽

Vol 14 (6) ◽

pp. e0218986 ◽

Cited By ~ 3

Author(s):

Mario Bianco ◽

Jarlene A. Lopes ◽

Hellen J. V. Beiral ◽

João D. D. Filho ◽

Stephan P. Frankenfeld ◽

...

Keyword(s):

Ureteral Obstruction ◽

Redox Homeostasis ◽

Unilateral Ureteral Obstruction ◽

Contralateral Kidney ◽

Mitochondrial Functions

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Cardiac mitochondrial plasticity and thermal sensitivity in a fish inhabiting an artificially heated ecosystem

Scientific Reports ◽

10.1038/s41598-019-54165-3 ◽

2019 ◽

Vol 9 (1) ◽

Cited By ~ 2

Author(s):

Nicolas Pichaud ◽

Andreas Ekström ◽

Sophie Breton ◽

Fredrik Sundström ◽

Piotr Rowinski ◽

...

Keyword(s):

Citrate Synthase ◽

Thermal Sensitivity ◽

Natural Habitat ◽

Perca Fluviatilis ◽

Adjacent Area ◽

Adaptive Responses ◽

Mitochondrial Functions ◽

The Baltic ◽

Laboratory Acclimation ◽

Environmental Warming

AbstractSome evidence suggests that cardiac mitochondrial functions might be involved in the resilience of ectotherms such as fish to environmental warming. Here, we investigated the effects of acute and chronic changes in thermal regimes on cardiac mitochondrial plasticity and thermal sensitivity in perch (Perca fluviatilis) from an artificially heated ecosystem; the “Biotest enclosure” (~25 °C), and from an adjacent area in the Baltic Sea with normal temperatures (reference, ~16 °C). We evaluated cardiac mitochondrial respiration at assay temperatures of 16 and 25 °C, as well as activities of lactate dehydrogenase (LDH) and citrate synthase (CS) in Biotest and reference perch following 8 months laboratory-acclimation to either 16 or 25 °C. While both populations exhibited higher acute mitochondrial thermal sensitivity when acclimated to their natural habitat temperatures, this sensitivity was lost when Biotest and reference fish were acclimated to 16 and 25 °C, respectively. Moreover, reference fish displayed patterns of metabolic thermal compensation when acclimated to 25 °C, whereas no changes were observed in Biotest perch acclimated to 16 °C, suggesting that cardiac mitochondrial metabolism of Biotest fish expresses local adaptation. This study highlights the adaptive responses of cardiac mitochondria to environmental warming, which can impact on fish survival and distribution in a warming climate.

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Numerical modelling of the effects of cold atmospheric plasma on mitochondrial redox homeostasis and energy metabolism

Scientific Reports ◽

10.1038/s41598-019-53219-w ◽

2019 ◽

Vol 9 (1) ◽

Cited By ~ 2

Author(s):

Tomoyuki Murakami

Keyword(s):

Energy Metabolism ◽

Cell Fate ◽

Cell Metabolism ◽

Redox Homeostasis ◽

Tca Cycle ◽

Adenosine Diphosphate ◽

Atmospheric Plasma ◽

Regulation System ◽

Acid Oxidation ◽

Mitochondrial Functions

AbstractA biochemical reaction model clarifies for the first time how cold atmospheric plasmas (CAPs) affect mitochondrial redox homeostasis and energy metabolism. Fundamental mitochondrial functions in pyruvic acid oxidation, the tricarboxylic acid (TCA) cycle and oxidative phosphorylation involving the respiratory chain (RC), adenosine triphosphate/adenosine diphosphate (ATP/ADP) synthesis machinery and reactive oxygen species/reactive nitrogen species (ROS/RNS)-mediated mechanisms are numerically simulated. The effects of CAP irradiation are modelled as 1) the influx of hydrogen peroxide (H$${}_{2}$$2O$${}_{2}$$2) to an ROS regulation system and 2) the change in mitochondrial transmembrane potential induced by RNS on membrane permeability. The CAP-induced stress modifies the dynamics of intramitochondrial H$${}_{2}$$2O$${}_{2}$$2 and superoxide anions, i.e., the rhythm and shape of ROS oscillation are disturbed by H$${}_{2}$$2O$${}_{2}$$2 infusion. Furthermore, CAPs control the ROS oscillatory behaviour, nicotinamide adenine dinucleotide redox state and ATP/ADP conversion through the reaction mixture over the RC, the TCA cycle and ROS regulation system. CAPs even induce a homeostatic or irreversible state transition in cell metabolism. The present computational model demonstrates that CAPs crucially affect essential mitochondrial functions, which in turn affect redox signalling, metabolic cooporation and cell fate decision of survival or death.

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A core of functionally complementary bacteria colonizes oysters in Pacific Oyster Mortality Syndrome

10.1101/2020.11.16.384644 ◽

2020 ◽

Author(s):

Aude Lucasson ◽

Xing Luo ◽

Shogofa Mortaza ◽

Julien de Lorgeril ◽

Eve Toulza ◽

...

Keyword(s):

Stress Responses ◽

Pacific Oyster ◽

Sulfur Metabolism ◽

Redox Homeostasis ◽

Bacterial Consortium ◽

Adaptive Responses ◽

Cell Defense ◽

Highly Active ◽

Sequence Of Events ◽

Oyster Mortality

ABSTRACTThe Pacific oyster Crassostrea gigas is one of the main cultivated invertebrate species around the world. Since 2008, oyster juveniles have been confronted with a lethal syndrome, Pacific Oyster Mortality Syndrome (POMS). The etiology of POMS is complex. Recently, we demonstrated that POMS is a polymicrobial disease. It is initiated by a primary infection with the herpesvirus OsHV-1 μ Var, and evolves towards a secondary fatal bacteremia that is enabled by the oyster’s immunocompromised state. In the present article, we describe the implementation of an unprecedented combination of metabarcoding and metatranscriptomic approaches to show that the sequence of events in POMS pathogenesis is conserved across infectious environments and susceptible oyster genetic backgrounds. We also identify a core colonizing bacterial consortium which, together with OsHV-1 μ Var, forms the POMS pathobiota. This bacterial core is characterized by highly active global metabolism and key adaptive responses to the within-host environment (e.g. stress responses and redox homeostasis). Several marine gamma proteobacteria in the core express different and complementary functions to exploit the host’s resources. Such cross-benefits are observed in colonization-related functions, and reveal specific strategies used by these bacteria to adapt and colonize oysters (e.g. adhesion, cell defense, cell motility, metal homeostasis, natural competence, quorum sensing, transport, and virulence). Interdependence and cooperation within the microbial community for metabolic requirements is best exemplified by sulfur metabolism, which is a property of the pathobiota as a whole and not of a single genus. We argue that this interdependence may dictate the conservation of the POMS pathobiota across distinct environments and oyster genetic backgrounds.

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The Atrophic Effect of 1,25(OH)2 Vitamin D3 (Calcitriol) on C2C12 Myotubes Depends on Oxidative Stress

Antioxidants ◽

10.3390/antiox10121980 ◽

2021 ◽

Vol 10 (12) ◽

pp. 1980

Author(s):

Tommaso Raiteri ◽

Ivan Zaggia ◽

Simone Reano ◽

Andrea Scircoli ◽

Laura Salvadori ◽

...

Keyword(s):

Skeletal Muscle ◽

Redox Homeostasis ◽

Antioxidant Properties ◽

Mitochondrial Metabolism ◽

C2c12 Myotubes ◽

Ros Production ◽

Muscle Loss ◽

Mitochondrial Functions ◽

Skeletal Muscle Loss ◽

The Impact

Dysfunctional mitochondrial metabolism has been linked to skeletal muscle loss in several physio-pathological states. Although it has been reported that vitamin D (VD) supports cellular redox homeostasis by maintaining normal mitochondrial functions, and VD deficiency often occurs in conditions associated with skeletal muscle loss, the efficacy of VD supplementation to overcome muscle wasting is debated. Investigations on the direct effects of VD metabolites on skeletal muscle using C2C12 myotubes have revealed an unexpected pro-atrophic activity of calcitriol (1,25VD), while its upstream metabolites cholecalciferol (VD3) and calcidiol (25VD) have anti-atrophic effects. Here, we investigated if the atrophic effects of 1,25VD on myotubes depend on its activity on mitochondrial metabolism. The impact of 1,25VD and its upstream metabolites VD3 and 25VD on mitochondria dynamics and the activity of C2C12 myotubes was evaluated by measuring mitochondrial content, architecture, metabolism, and reactive oxygen species (ROS) production. We found that 1,25VD induces atrophy through protein kinase C (PKC)-mediated ROS production, mainly of extramitochondrial origin. Consistent with this, cotreatment with the antioxidant N-acetylcysteine (NAC), but not with the mitochondria-specific antioxidant mitoTEMPO, was sufficient to blunt the atrophic activity of 1,25VD. In contrast, VD3 and 25VD have antioxidant properties, suggesting that the efficacy of VD supplementation might result from the balance between atrophic pro-oxidant (1,25VD) and protective antioxidant (VD3 and 25VD) metabolites.

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Element and redox homeostasis in rats after red wine consumption

Zeitschrift für Gastroenterologie ◽

10.1055/s-0031-1278515 ◽

2011 ◽

Vol 49 (05) ◽

Author(s):

K Szentmihályi ◽

Z May ◽

H Fébel ◽

G Bekő ◽

A Blázovics

Keyword(s):

Red Wine ◽

Redox Homeostasis ◽

Wine Consumption

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