About this Research Topic
Intracellular oxidative stress is induced by the overexpression of reactive oxygen species (ROS) and decreased antioxidants defense activity, causing deleterious chemical changes in biomolecules such as lipids, DNA, RNA, and proteins. ROS are the highly-reactive, oxygen-containing, radical or molecular species that include superoxide anion/radical (O2•‒), hydrogen peroxide (H2O2) and hydroxyl radical (HO• ). Chemically, ROS are generated from molecular oxygen (O2) during the successive 4 steps of one electron reduction in mitochondrial respiratory chain. Free radicals (O2•‒/HO• ) can further react with organic substrates to form intermediate species and yield the secondary ROS, such as peroxyl radical (RO2•) and hydroperoxide (ROOH). H2O2, which is a relatively less toxic but more stable molecular species, becomes highly toxic after further interaction with Fe++ (Fenton reaction) or in presence of O2 •‒ (Haber-Weiss reaction).
About 90% of the endogenous ROS are generated during oxidative phosphorylation in the mitochondria which are the powerhouses to provide energy to cell in the form of ATP molecules, in order to fuel biochemical reactions and support biological functions. In addition to the ATP synthesis and ROS production/scavenging, mitochondria also regulate intracellular Ca2+, apoptotic cell death, and activation of the caspase family of proteases. ROS accumulation, whether from overproduction or as a sequel to defective antioxidant enzymes may lead to the irreversible damage to mitochondria, which may induce or exacerbate pathologies across a wider spectrum of metabolic and inflammatory diseases. The goal is to enhance our understanding how the ROS play out in physiology and pathophysiology, and how the ROS imbalance may influence the cellular or tissue homeostasis and critical cellular processes, such as aerobic/anaerobic respiration, β-oxidation, fatty acid synthesis, protein translation and post-translational modifications, and other modifications driving the genetic/epigenetic landscape reprogramming in metabolic and inflammatory diseases.
Obesity triggers the risk of metabolic syndromes including hypertension, type 2 diabetes and related morbidities such as hypertension, atherosclerosis, NAFLD/NASH, stroke, cardiovascular disease, aging, neurodegenerative diseases, certain types of cancers, and other chronic inflammatory conditions. Over the past years, significant progress has been made toward developing therapeutic strategies, pharmacological interventions, and mitochondria-targeted approaches that reduce oxidative stress and mitochondrial damage or dysfunction and improve mitochondrial quality in disease setting. The purpose of this special issue is to highlight the recent advances and progress on the mechanisms of ROS-mediated oxidative stress and novel therapeutic strategies used in metabolic and inflammatory diseases.
We, therefore, welcome Original Research, Review, Mini Review and Perspective articles on the above-mentioned pathophysiological changes in the setting of: Obesity; Type-2 Diabetes; Hypertension; NAFLD/NASH; Stroke; Atherosclerosis; Cardiovascular disease; Aging and age-related neurodegenerative diseases; and other chronic inflammatory conditions.
About 90% of the endogenous ROS are generated during oxidative phosphorylation in the mitochondria which are the powerhouses to provide energy to cell in the form of ATP molecules, in order to fuel biochemical reactions and support biological functions. In addition to the ATP synthesis and ROS production/scavenging, mitochondria also regulate intracellular Ca2+, apoptotic cell death, and activation of the caspase family of proteases. ROS accumulation, whether from overproduction or as a sequel to defective antioxidant enzymes may lead to the irreversible damage to mitochondria, which may induce or exacerbate pathologies across a wider spectrum of metabolic and inflammatory diseases. The goal is to enhance our understanding how the ROS play out in physiology and pathophysiology, and how the ROS imbalance may influence the cellular or tissue homeostasis and critical cellular processes, such as aerobic/anaerobic respiration, β-oxidation, fatty acid synthesis, protein translation and post-translational modifications, and other modifications driving the genetic/epigenetic landscape reprogramming in metabolic and inflammatory diseases.
Obesity triggers the risk of metabolic syndromes including hypertension, type 2 diabetes and related morbidities such as hypertension, atherosclerosis, NAFLD/NASH, stroke, cardiovascular disease, aging, neurodegenerative diseases, certain types of cancers, and other chronic inflammatory conditions. Over the past years, significant progress has been made toward developing therapeutic strategies, pharmacological interventions, and mitochondria-targeted approaches that reduce oxidative stress and mitochondrial damage or dysfunction and improve mitochondrial quality in disease setting. The purpose of this special issue is to highlight the recent advances and progress on the mechanisms of ROS-mediated oxidative stress and novel therapeutic strategies used in metabolic and inflammatory diseases.
We, therefore, welcome Original Research, Review, Mini Review and Perspective articles on the above-mentioned pathophysiological changes in the setting of: Obesity; Type-2 Diabetes; Hypertension; NAFLD/NASH; Stroke; Atherosclerosis; Cardiovascular disease; Aging and age-related neurodegenerative diseases; and other chronic inflammatory conditions.
Keywords: Oxidative stress, ROS, Mitochondrial impairment, Metabolic inflammatory diseases
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