Choose an application

• Reference Manager
• EndNote
• RefWorks (Direct export to RefWorks)

Our common knowledge on oxidative stress has evolved substantially over the years and has been mostly focused on the fundamental chemical reactions and the most relevant chemical species involved in the human pathophysiology of oxidative stress-associated diseases. Thus, reactive oxygen species and reactive nitrogen species (ROS and RNS) were identified as the key players initiating, mediating, and regulating the cellular and biochemical complexity of oxidative stress either as physiological (acting pro-hormetic) or as pathogenic (causing destructive vicious circle) process. The papers published in this particular Special Issue of the Cells demonstrate the impressive pathophysiological relevance of ROS and RNS in a range of contexts, including the relevance of second messengers of free radicals like 4-hydroxynonenal, allowing us to assume that even more detailed mechanisms of their positive and negative effects lie in wait, and should assist in better monitoring of the major modern diseases and the development of advanced integrative biomedicine treatments.

toxicity --- toll-like receptors --- acrolein --- hydroxyapatite-based biomaterials --- LC-MS/MS --- blood–brain barrier --- NADPH-oxidase --- human neuroblastoma SH-SY5Y cells --- NRF2-NQO1 axis --- granulocytes --- free radicals --- antioxidant --- plaque vulnerability --- bEnd.3 --- relaxation --- Ca2+ --- keratinocytes --- oxidative metabolism of the cells --- lipid peroxidation --- intermittent hypoxia --- osteoblast growth --- UV radiation --- ROS --- bEnd5 --- cyclopurines --- NF?B --- glucose deprivation --- antimicrobial --- endothelial cells --- 4-hydroxynonenal (4-HNE) --- histamine --- glutamine deprivation --- optical coherence tomography --- antioxidants --- DNA damage --- glutathione --- NQO1 transcript variants --- xeroderma pigmentosum --- cancer cells --- VAS2870 --- reactive oxygen species (ROS) --- TP53 mutation --- DNA and RNA polymerases --- viability --- oxidative burst --- macrophages --- inflammation --- Nrf2 --- von Willebrand factor --- reactive oxygen species --- growth control --- intracellular signaling --- MFN2 --- nuclear factor erythroid 2–related factor 2 --- fusion/fission --- IMR-90 --- calcium --- proliferation --- mitochondria --- pathophysiology of oxidative stress --- redox balance --- 4-hydroxynonenal --- cannabidiol --- oxidative homeostasis --- rs1800566 --- neuronal cell death --- heme-oxygenase-1 --- vitamins --- cell signaling --- TRPM2 channel --- aorta --- cancer --- growth --- cancer regression --- oxidative stress --- nucleotide excision repair

Choose an application

• Reference Manager
• EndNote
• RefWorks (Direct export to RefWorks)

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