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Reactive oxygen species (ROS) are produced by healthy cells and are maintained at physiological levels by antioxidant systems. However, when ROS increase in number, a condition of oxidative stress occurs, leading to many human diseases, including cancer. The relationship between oxidative stress and cancer is complex since ROS play a double-edged role in cancer development and under therapy response. This paradox represents a great challenge for researchers and needs to be investigated. The articles collected in this Special Issue can help to clarify the role of ROS modulation in cancer prevention and treatment, and to dissect the molecular mechanisms underlying its paradoxical role in order to counteract carcinogenesis or enhance sensitivity to anticancer therapy.

Medicine --- Oncology --- sonodynamic therapy --- carbon doped titanium dioxide --- sonosensitizers --- ultrasound --- cancer treatment --- breast cancer treatment --- radiotherapy --- hematological malignancies --- oxidative stress --- lymphoma --- leukemia --- multiple myeloma --- apoptosis --- mitochondria --- ultraviolet-C (UVC) --- withanolide --- combined treatment --- oral cancer --- DNA damage --- cancer therapy --- immune system --- Hypericum perforatum --- hyperforin --- reactive oxygen species --- pH regulation --- tumor prevention --- tumor therapy --- cancerogenesis --- inflammatory signaling --- natural compounds --- pancreatic cancer --- antitumor agents --- coordination polymers --- bioinorganic chemistry --- cold atmospheric plasma --- reactive oxygen and nitrogen species --- nitrite --- cancer stem cells --- chemoresistance --- glutathione --- lipid peroxidation --- ZEB-1 --- GPX4 --- ferroptosis --- HO-1 --- Nrf2 --- cancer progression --- patients --- therapy --- prognosis --- biomarker --- Eprenetapopt --- Erastin --- glutathione (GSH) --- SLC7A11 --- iron --- NRF2 --- n/a

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Reactive oxygen species (ROS) are produced by healthy cells and are maintained at physiological levels by antioxidant systems. However, when ROS increase in number, a condition of oxidative stress occurs, leading to many human diseases, including cancer. The relationship between oxidative stress and cancer is complex since ROS play a double-edged role in cancer development and under therapy response. This paradox represents a great challenge for researchers and needs to be investigated. The articles collected in this Special Issue can help to clarify the role of ROS modulation in cancer prevention and treatment, and to dissect the molecular mechanisms underlying its paradoxical role in order to counteract carcinogenesis or enhance sensitivity to anticancer therapy.

Medicine --- Oncology --- sonodynamic therapy --- carbon doped titanium dioxide --- sonosensitizers --- ultrasound --- cancer treatment --- breast cancer treatment --- radiotherapy --- hematological malignancies --- oxidative stress --- lymphoma --- leukemia --- multiple myeloma --- apoptosis --- mitochondria --- ultraviolet-C (UVC) --- withanolide --- combined treatment --- oral cancer --- DNA damage --- cancer therapy --- immune system --- Hypericum perforatum --- hyperforin --- reactive oxygen species --- pH regulation --- tumor prevention --- tumor therapy --- cancerogenesis --- inflammatory signaling --- natural compounds --- pancreatic cancer --- antitumor agents --- coordination polymers --- bioinorganic chemistry --- cold atmospheric plasma --- reactive oxygen and nitrogen species --- nitrite --- cancer stem cells --- chemoresistance --- glutathione --- lipid peroxidation --- ZEB-1 --- GPX4 --- ferroptosis --- HO-1 --- Nrf2 --- cancer progression --- patients --- therapy --- prognosis --- biomarker --- Eprenetapopt --- Erastin --- glutathione (GSH) --- SLC7A11 --- iron --- NRF2

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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