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Poised at the convergence of most catabolic and anabolic pathways, mitochondria are the center of heterotrophic aerobic life, representing a hub in the overall metabolic network of cells. The energetic functions performed by mitochondria face the unavoidable redox hurdle of handling huge amounts of oxygen while keeping its own as well as the cellular redox environment under control. Reactive oxygen species (ROS) are produced in the respiratory chain as a result of the energy supplying function of mitochondria. Originally considered an unavoidable by-product of oxidative phosphorylation, ROS have become crucial signaling molecules when their levels are kept within physiological range. This occurs when their production and scavenging are balanced within mitochondria and cells. Mitochondria-generated hydrogen peroxide can act as a signaling molecule within mitochondria or in the cytoplasm, affecting multiple networks that control, for example, cell cycle, stress response, cell migration and adhesion, energy metabolism, redox balance, cell contraction, and ion channels. However, under pathophysiological conditions, excessive ROS levels can happen due to either overproduction, overwhelming of antioxidant defenses, or both. Under oxidative stress, detrimental effects of ROS include oxidation of protein, lipids, and nucleic acids; mitochondrial depolarization and calcium overload; and cell-wide oscillations mediated by ROS-induced ROS release mechanisms. Mitochondrial dysfunction is central in the pathogenesis of numerous human maladies including cardiomyopathies and neurodegeneration. Diseases characterized by altered nutrient metabolism, such as diabetes and cancer, exhibit elevated ROS levels. These may contribute to pathogenesis by increasing DNA mutation, affecting regulatory signaling and transcription, and promoting inflammation. Under metabolic stress, several ionic channels present in the inner and outer mitochondrial membranes can have pro-life and -death effects. In the present E-book, based on the Frontiers Research Topic entitled: "Mitochondria: Hubs of cellular signaling, energetics and redox balance", we address one of the fundamental questions that the field of ROS biology faces today: how do mitochondria accomplish a reliable energy provision and at the same time keep ROS levels within physiological, non-harming, limits but crucial for cellular signaling function? Additionally, and within the perspective of mitochondria as signaling-energetic hubs in the extensive cellular metabolic network, we ask how can their collective dynamics scale from the subcellular to the cellular, tissue and organ levels to affect function in health and disease.

redox and energetic compartmentation --- light- and anesthetics-induced cardioprotection --- redox metabolism and signaling --- hypertrophic and diabetic cardiomyopathies --- skeletal-cardiac muscle and brain protection --- ketone bodies --- post-translational modifications --- redox aging --- lipid catabolism --- necroptosis

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Poised at the convergence of most catabolic and anabolic pathways, mitochondria are the center of heterotrophic aerobic life, representing a hub in the overall metabolic network of cells. The energetic functions performed by mitochondria face the unavoidable redox hurdle of handling huge amounts of oxygen while keeping its own as well as the cellular redox environment under control. Reactive oxygen species (ROS) are produced in the respiratory chain as a result of the energy supplying function of mitochondria. Originally considered an unavoidable by-product of oxidative phosphorylation, ROS have become crucial signaling molecules when their levels are kept within physiological range. This occurs when their production and scavenging are balanced within mitochondria and cells. Mitochondria-generated hydrogen peroxide can act as a signaling molecule within mitochondria or in the cytoplasm, affecting multiple networks that control, for example, cell cycle, stress response, cell migration and adhesion, energy metabolism, redox balance, cell contraction, and ion channels. However, under pathophysiological conditions, excessive ROS levels can happen due to either overproduction, overwhelming of antioxidant defenses, or both. Under oxidative stress, detrimental effects of ROS include oxidation of protein, lipids, and nucleic acids; mitochondrial depolarization and calcium overload; and cell-wide oscillations mediated by ROS-induced ROS release mechanisms. Mitochondrial dysfunction is central in the pathogenesis of numerous human maladies including cardiomyopathies and neurodegeneration. Diseases characterized by altered nutrient metabolism, such as diabetes and cancer, exhibit elevated ROS levels. These may contribute to pathogenesis by increasing DNA mutation, affecting regulatory signaling and transcription, and promoting inflammation. Under metabolic stress, several ionic channels present in the inner and outer mitochondrial membranes can have pro-life and -death effects. In the present E-book, based on the Frontiers Research Topic entitled: "Mitochondria: Hubs of cellular signaling, energetics and redox balance", we address one of the fundamental questions that the field of ROS biology faces today: how do mitochondria accomplish a reliable energy provision and at the same time keep ROS levels within physiological, non-harming, limits but crucial for cellular signaling function? Additionally, and within the perspective of mitochondria as signaling-energetic hubs in the extensive cellular metabolic network, we ask how can their collective dynamics scale from the subcellular to the cellular, tissue and organ levels to affect function in health and disease.

redox and energetic compartmentation --- light- and anesthetics-induced cardioprotection --- redox metabolism and signaling --- hypertrophic and diabetic cardiomyopathies --- skeletal-cardiac muscle and brain protection --- ketone bodies --- post-translational modifications --- redox aging --- lipid catabolism --- necroptosis

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Mitochondria are subcellular organelles evolved by the endosymbiosis of bacteria with eukaryotic cells. They are the main source of ATP in the cell and engaged in other aspects of cell metabolism and cell function, including the regulation of ion homeostasis, cell growth, redox status, and cell signaling. Due to their central role in cell life and death, mitochondria are also involved in the pathogenesis and progression of human diseases/conditions, including neurodegenerative and cardiovascular disorders, cancer, diabetes, inflammation, and aging. However, despite the increasing number of studies, precise mechanisms whereby mitochondria are involved in the regulation of basic physiological functions, as well as their role in the cell under pathophysiological conditions, remain unknown. A lack of in-depth knowledge of the regulatory mechanisms of mitochondrial metabolism and function, as well as interplay between the factors that transform the organelle from its role in pro-survival to pro-death, have hindered the development of new mitochondria-targeted pharmacological and conditional approaches for the treatment of human diseases. This book highlights the latest achievements in elucidating the role of mitochondria under physiological conditions, in various cell/animal models of human diseases, and in patients.

Medicine --- hypoglycemia --- sodium dichloroacetate --- pyruvate dehydrogenase kinase --- pyruvate dehydrogenase --- oxidative stress --- neuron death --- cholangiocellular carcinoma --- mitochondria --- energy metabolism --- oxidative phosphorylation --- 4-HNE --- DRP1 --- ERK1/2 --- hippocampus --- JNK --- mitochondrial dynamics --- PKA --- protein phosphatases --- TUNEL --- DDE --- high-fat diet --- mitochondrial UCP2 --- ROS --- antioxidant system --- uncoupling protein --- mitochondria: energy metabolism --- lipid handling --- fatty acid oxidation --- potassium channel --- reactive oxygen species --- antioxidants --- life span --- aging --- BKCa channels --- pravastatin --- gemfibrozil --- liver --- colon --- mitochondrial function --- cyclosporin A --- mitochondria calcium buffering --- mitochondria bioenergetics --- mitochondria permeability transition pore --- inorganic phosphate --- hepatic fibrogenesis --- HtrA2/Omi --- reactive oxygen species stress --- mitochondrial homeostasis --- complex I (CI) deficiency --- metabolome and proteome profiling --- reactive oxygen species (ROS) --- respirasome assembly --- electron tunneling (ET) --- perilipin 5 --- lipid droplet --- H9c2 cardiomyoblasts --- adenine nucleotide translocase --- respiratory supercomplexes --- ETC complexes --- dentate granule cell --- epilepsy --- hyperforin --- LONP1 --- neuroprotection --- pilocarpine --- seizure --- siRNA --- cardioprotection --- mitochondrial permeability transition pores --- mitochondrial connexin 43 --- cardiolipin --- iron overload --- hepcidin --- transferrin --- ferritin --- ZIP --- inflammation --- mtDNA --- mitochondrial dysfunction --- muscle aging --- physical performance --- LHON --- Siberian population --- ancient mutation --- specific genetic background --- apoptosis --- human amniotic membrane --- mitochondrial cell death --- BAX --- BCL-2 --- tensile strength --- mitochondrial gene expression --- mtDNA transcription --- mtRNA --- post-transcriptional mtRNA processing --- dsRNA --- innate immunity --- interferon response --- amino acid neurotransmitter --- cerebellar amino acid metabolism --- hypoxia --- 2-oxoglutarate dehydrogenase --- tricarboxylic acid cycle --- heart --- cytoskeletal proteins --- mitochondrial interactions --- plectin --- tubulin beta --- signaling --- GW9662 --- ischemia reperfusion injury --- Langendorff --- myocardial --- pioglitazone --- redox state --- rosiglitazone --- TZD --- uncoupling --- ADP/ATP carrier --- KmADP --- dextran --- morphology --- cardiomyocytes --- telomere length --- telomerase activity --- development --- regeneration --- intranuclear mitochondria --- healthy cells --- electron and confocal microscopy --- signaling pathways --- ion homeostasis --- human diseases

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Antioxidants in food have a dual role; on the one hand, they preserve the quality and shelf life of food products; on the other hand, they function as an external aid, helping to defend our living cells from the threat of oxidative stress. Therefore, foods rich in antioxidants are a useful tool to reduce morbidity and prevent degenerative diseases. Consequently, research related to antioxidants is continually growing. This book brings together 21 articles regarding the latest advances in the most relevant fields of food antioxidant research; from the identification and characterization of new active components, to their molecular mechanisms and the scientific evidence of their clinical use and effectiveness.

Research & information: general --- Biology, life sciences --- Food & society --- green tea extract --- food processing --- tannase --- ultrasound --- antioxidant activity --- liver injury --- acclimatisation --- antioxidant defences --- chlorophyll fluorescence --- in vitro culture --- peroxidase --- stevia plants --- 7S basic globulins --- anti-inflammatory protein --- antioxidant protein --- cytokines --- glutathione --- iNOS --- nitric oxide --- oxidative stress --- sweet lupins group --- home-cooking --- extra virgin olive oil --- UPLC-ESI-QqQ-MS/MS --- healthy cooking --- Mediterranean diet --- phenolic compounds --- bioactive compounds --- functional pasta --- gluten-free pasta --- bioaccessibility --- bioavailability --- whole grain --- composite flour --- legumes --- food by-products --- avocados (Persea americana Mill.) --- low temperatures --- plastochromanol-8 --- tocotrienols --- tocopherols --- tocochromanols --- kombucha --- tea --- fermentation --- antioxidant --- flavonoids --- polyphenols --- ascorbic acid --- chlorophyll and carotenoid content --- biodiversity --- Capsicum annuum L. --- β-carotene --- statistical analysis --- rye bread --- microencapsulation --- phenolics --- in vitro relative bioaccessibility --- lipoxygenase --- cyclooxygenase --- acetylcholinesterase --- biological activity --- lycopene --- antioxidants --- cancer --- diabetes --- cardiovascular diseases --- skin disorders --- free radicals --- spectrophotometer --- limitations --- chemical reactions --- colorimetry --- anthraquinone --- free radical scavenging --- inflammatory cytokines --- apoptosis --- Rumex crispus --- skins --- seeds --- Vitis vinifera --- cyclic voltammetry --- anthocyanin metabolites --- cardioprotection --- hepatoprotection --- nephroprotection --- neuroprotection --- antioxidant peptides --- element of pork carcasses --- spectrometric analysis --- ascorbate --- ascorbate–glutathione cycle --- capsaicin --- catalase --- dihydrocapsaicin --- NADP-dehydrogenases --- superoxide dismutase --- red cabbage --- in vitro gastrointestinal digestion --- acid-resistant capsule --- UHPLC-Q-Orbitrap HRMS --- apples --- reducing and chelating capacity --- HPLC–DAD–MS/MS --- Dillenia indica --- heme oxygenase 1 (HO-1) --- nuclear factor erythroid 2-related factor 2 (Nrf2) --- RAW 264.7 cells --- apo-carotenals --- bone --- osteoclasts --- NFκB --- synergy --- n/a --- ascorbate-glutathione cycle --- HPLC-DAD-MS/MS

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Antioxidants in food have a dual role; on the one hand, they preserve the quality and shelf life of food products; on the other hand, they function as an external aid, helping to defend our living cells from the threat of oxidative stress. Therefore, foods rich in antioxidants are a useful tool to reduce morbidity and prevent degenerative diseases. Consequently, research related to antioxidants is continually growing. This book brings together 21 articles regarding the latest advances in the most relevant fields of food antioxidant research; from the identification and characterization of new active components, to their molecular mechanisms and the scientific evidence of their clinical use and effectiveness.

Research & information: general --- Biology, life sciences --- Food & society --- green tea extract --- food processing --- tannase --- ultrasound --- antioxidant activity --- liver injury --- acclimatisation --- antioxidant defences --- chlorophyll fluorescence --- in vitro culture --- peroxidase --- stevia plants --- 7S basic globulins --- anti-inflammatory protein --- antioxidant protein --- cytokines --- glutathione --- iNOS --- nitric oxide --- oxidative stress --- sweet lupins group --- home-cooking --- extra virgin olive oil --- UPLC-ESI-QqQ-MS/MS --- healthy cooking --- Mediterranean diet --- phenolic compounds --- bioactive compounds --- functional pasta --- gluten-free pasta --- bioaccessibility --- bioavailability --- whole grain --- composite flour --- legumes --- food by-products --- avocados (Persea americana Mill.) --- low temperatures --- plastochromanol-8 --- tocotrienols --- tocopherols --- tocochromanols --- kombucha --- tea --- fermentation --- antioxidant --- flavonoids --- polyphenols --- ascorbic acid --- chlorophyll and carotenoid content --- biodiversity --- Capsicum annuum L. --- β-carotene --- statistical analysis --- rye bread --- microencapsulation --- phenolics --- in vitro relative bioaccessibility --- lipoxygenase --- cyclooxygenase --- acetylcholinesterase --- biological activity --- lycopene --- antioxidants --- cancer --- diabetes --- cardiovascular diseases --- skin disorders --- free radicals --- spectrophotometer --- limitations --- chemical reactions --- colorimetry --- anthraquinone --- free radical scavenging --- inflammatory cytokines --- apoptosis --- Rumex crispus --- skins --- seeds --- Vitis vinifera --- cyclic voltammetry --- anthocyanin metabolites --- cardioprotection --- hepatoprotection --- nephroprotection --- neuroprotection --- antioxidant peptides --- element of pork carcasses --- spectrometric analysis --- ascorbate --- ascorbate–glutathione cycle --- capsaicin --- catalase --- dihydrocapsaicin --- NADP-dehydrogenases --- superoxide dismutase --- red cabbage --- in vitro gastrointestinal digestion --- acid-resistant capsule --- UHPLC-Q-Orbitrap HRMS --- apples --- reducing and chelating capacity --- HPLC–DAD–MS/MS --- Dillenia indica --- heme oxygenase 1 (HO-1) --- nuclear factor erythroid 2-related factor 2 (Nrf2) --- RAW 264.7 cells --- apo-carotenals --- bone --- osteoclasts --- NFκB --- synergy --- n/a --- ascorbate-glutathione cycle --- HPLC-DAD-MS/MS