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This eBook is a collection of articles from a Frontiers Research Topic. Frontiers Research Topics are very popular trademarks of the Frontiers Journals Series: they are collections of at least ten articles, all centered on a particular subject. With their unique mix of varied contributions from Original Research to Review Articles, Frontiers Research Topics unify the most influential researchers, the latest key findings and historical advances in a hot research area! Find out more on how to host your own Frontiers Research Topic or contribute to one as an author by contacting the Frontiers Editorial Office: frontiersin.org/about/contact
thermogenesis --- mitochondria --- uncoupling proteins (UCPs) --- obesity --- metabolic disease --- adipocytes --- dietary components
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Alteration in adequate energy balance maintenance results in serious disturbances such as obesity and its related metabolic disorders. In Mammals, energy balance is homeostatically controlled through hormonal and neuroendocrine systems which cooperation is based on cross-talk between central and peripheral signals. The hypothalamus as well as peripheral hormones among which adipokines from adipose tissue and thyroid hormones play a crucial role in energy homeostasis. Unraveling the physiological, cellular and molecular mechanisms through which hormonal and neuroendocrine systems regulate energy balance has been a long-standing challenge in biology and is now more necessary when considering the world-wide increasing prevalence of obesity. Indeed, recognizing and understanding the biochemical and nutrient signaling pathways contributing to the nervous and endocrine integration of physiological mechanisms involved in the normal and/or abnormal regulation of energy balance is fundamental also to the development of new, effective, and targeted treatments for obesity. Recent studies have highlighted the role of hypothalamic pro-opiomelanocortin-expressing neurons in the regulation of energy homeostasis by controlling energy expenditure and food intake. This is accomplished through a precise balance of production and degradation of a-melanocyte-stimulating hormone, an anorexigenic neuropeptide which is degraded to an inactive form unable to inhibit food intake by the key enzyme prolyl carboxypeptidase (PRCP), thus suggesting that pharmacologic approaches targeting PRCP may provide a novel and effective option for the management of obesity and its associated metabolic disorders. Indeed, efforts have been made to generate potent, brain-penetrant PRCP inhibitors. Weight loss due to negative energy balance is a goal for obese subjects not always reachable by dietary caloric restriction or increased physical activity. Lipid-lowering therapies have been suggested to have potential benefits, however, the establishment of comprehensive therapeutic strategies is still awaited. Recently, it has been reported that thyroid hormone (TH)- derivatives such as 3,5-diiodothyronine and 3-iodothyronamine possess interesting biological activities, opening new perspectives in thyroid physiology and TH derivatives therapeutic usage. Moreover, several studies, focusing on the interaction between thyroid hormone (TH), the autonomic nervous system and the liver, revealed an important role for the hypothalamus in the differential effects of TH on autonomic outflow to peripheral organs controlling energy balance. This Research Topic aims to give a comprehensive and integrate view of the factors involved in the endocrine and neuroendocrine signaling in energy balance regulation to highlight their involvement into physiological processes and regulatory systems as well as their perturbation during pathological processes.
Uncoupling --- Mitochondria --- catch up fat --- brown adipose tissue --- Thyroid Hormones --- Lipid Metabolism --- energy balance --- Apelin --- melanocortin --- Adipogenesis
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The kidney performs important functions in the human body and can inflict either acute kidney injury (AKI) or chronic kidney disease (CKD). AKI can be induced by kidney ischemia, drugs such as cisplatin, and heavy metals such as cadmium and arsenic. CKD can be induced by drugs, heavy metals, hypertension, and diabetes, as well as cancer. Importantly, nearly all kidney disorders have been shown to involve redox imbalance, reductive stress, oxidative stress, and mitochondrial abnormalities such as impaired mitochondrial homeostasis, including disrupted mitophagy and deranged mitochondrial unfolded protein responses. Understanding how these redox-related dysregulated pathways operate may give us new insights into how to design novel approaches to fighting kidney disease. This Special Issue of Biomolecules entitled “Redox imbalance and mitochondrial abnormalities in kidney disease” covers a variety of topics focusing on oxidative stress, mitochondrial dysfunction, and antioxidation enhancement implicated in kidney disease or kidney transplantation.
diabetic kidney disease --- caloric restriction --- NADH/NAD+ --- redox imbalance --- mitochondrial homeostasis --- mitophagy --- oxidative stress --- kidney allograft --- kidney rejection --- ischemia --- acute kidney injury (AKI) --- chronic kidney disease (CKD) --- tricarboxylic acid (TCA) cycle --- mitochondrial metabolism --- mitochondrial redox signaling --- mitochondrial proteins --- oxidative phosphorylation (OXPHOS) --- fatty acid (FA) β-oxidation --- mitochondrial dynamics --- biogenesis --- diabetes --- kidney --- mitochondria --- Oryza sativa --- rice husk --- TCA cycle metabolites --- kidney diseases --- renalase --- chronic kidney disease --- major adverse cardiovascular outcomes --- cadmium --- kidney injury --- renal toxicity --- oxidative damage --- proximal tubule --- controlled oxygenated rewarming --- mitochondrial uncoupling --- rewarming injury --- temperature paradox --- redox --- mitochondrial dysfunction --- SGLT2 --- mitochondrial reactive oxygen species --- Warburg effect --- podocytopathies --- mitochondrial oxidative stress --- reactive oxygen species (ROS) --- antioxidant defense --- cell death --- n/a
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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.
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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Obesity and related co-morbidities are increasing worldwide and pose a serious health problem. Changes in lifestyle and diet would be the best remedies to fight obesity; however, many people will still rely on medical aid. Marine organisms have been prolific in the production of bioactive compounds for many diseases, e.g., cancer, and promise to be an excellent source for natural-derived molecules and novel nutraceuticals. Bioactive compounds with beneficial activities towards obesity have been described from diverse marine organism including marine algae, bacteria, sponges, fungi, crustaceans or fish. This Special Issue will highlight the progress in the following topics: Bioactive compounds for the treatment of obesity and obesity-related co-morbidities (diabetes, fatty liver, hyperlipidemia) from marine organisms; the isolation of novel compounds, the bioactivity screening of marine organisms and the elucidation of molecular mode of action of marine bioactive compounds.
natural compounds --- anti-obesity drugs --- high fat diet --- Ishige okamurae --- fat --- zebrafish Nile red fat metabolism assay --- physical exercise --- JAK2-STAT3 --- metabolite profiling --- obesity --- chlorophyll derivatives --- brown seaweed --- Skate skin --- PPAR? --- marine alga --- marine biodiscovery --- skate skin --- lipolytic --- leptin --- uncoupling protein 1 --- 3T3-L1 cells --- glucolipid metabolism disorder --- nutrition --- bioactivity --- chitosan oligosaccharide --- diphlorethohydroxycarmalol (DPHC) --- nutraceuticals --- whole small animal models --- high-fat diet --- adipocyte --- dyslipidemia --- bioactivity screening --- peroxisome proliferator-activated receptor gamma --- white adipose tissue --- antiobesity --- fatty liver disease --- thermal proteome profiling --- inflammation --- cyanobacteria --- Raja kenojei --- Arthrospira maxima --- cellularity --- adipocytes --- bioactive compound --- collagen peptide --- double-blind --- bisabolane-related compounds --- proliferation --- fatty acid metabolism --- cholesterol metabolism --- collagen --- randomized controlled trial --- mechanisms of action --- murine pre-adipocytes --- adipogenesis --- fucan --- marine sponges --- label-free quantitative proteomics --- diabetes --- body fat
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Lipids represent the major players in marine organisms as the major constituents of biological membranes, with key roles in biological processes and acclimation to environmental changes. New research trends aim to contribute to improving knowledge on the role lipids in the biological matrix, understanding the impact of climate change in marine organisms, and developing new tools for chemophenotyping, traceability, and biomarkers of trophic chains in marine ecosystems, such that the nutritional value or prospective bioactive compounds can be disclosed for health applications. “Lipids in the Ocean 2021” (http://lipids2021.web.ua.pt) was originally planned to be held at the University of Aveiro and ran from 5 to 7 July 2021 (and was ultimately an online conference due to uncertainties regarding the COVID-19 situation). The aim was to go in deep into research interests covering topics related to lipids from marine organisms, such as marine lipidomics, lipids as biomarkers in trophic webs, green lipids from the ocean (seaweeds, microalgae, and macrophytes), marine lipid biotechnology, and seafood traceability using lipids—from basic research to sustainable production and applications in the food, nutraceutics, feed, cosmetics, and pharma industries. This Special Issue welcomed not only attendees of “Lipids in the Ocean 2021” to publish their latest research outcomes but also all researchers in relevant fields to share their exciting works with the community.
fatty acids --- fungal endophytes --- laminariales --- Paradendryphiella salina --- brown adipose tissue --- browning --- energy expenditure --- n-3 fatty acid --- uncoupling protein --- white adipose tissue --- krill oil --- omega-3 polyunsaturated fatty acids --- bioavailability --- nutraceuticals --- dietary supplements --- dietary resource --- Mytilus galloprovincialis --- Crassostrea gigas --- diatom --- competition --- biofouling --- EPA --- DHA --- aquafeeds --- n-3/n-6 ratio --- n-3 PUFA --- IMTA --- powdered fish oil --- docosahexaenoic acid --- chitosan nanoparticles --- encapsulation efficiency --- loading capacity --- TGA --- FTIR --- oxidative stability --- algae --- bioactivity --- glycolipids --- lipidomics --- macroalgae --- phospholipids --- seaweeds --- long-chain PUFA synthesis --- desaturases --- elongases --- PKS pathway --- 20:5n-3 (EPA) --- 22:6n-3 (DHA) --- Tisochrysis lutea --- 13C artificial enrichment --- Crypthecodinium cohnii --- omega-3 fatty acid --- biomass recycling --- dinoflagellate extract --- FTIR spectroscopy --- Krebs cycle --- central metabolism --- kinetic model --- constraint-based model
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Dear colleagues, This Special Issue, “Endothelial Dysfunction: From Pathophysiology to Novel Therapeutic Approaches”, focuses on the pathophysiology of endothelial dysfunction, new biomarkers for endothelial dysfunction related to cardiovascular disorders or tumors, and novel therapeutic approaches for endothelial dysfunctions. Vascular endothelium is an active tissue and plays a crucial role in the maintenance of vascular homeostasis. Chronic exposure to risk factors, such as hypertension, high cholesterolemia, or oxidative stress, induces endothelial dysfunctions and results in a loss of endothelial integrity, smooth muscle cell proliferation, and macrophage recruitment. The pathophysiology of endothelial dysfunction (ED) is complex and multi-factorial factors are involved, such as oxidative stress or chronic inflammation. The primary prevention of cardiovascular risk factors and endothelial dysfunctions, as well as the early detection of or molecular imaging techniques for endothelial dysfunction, helps to prevent the development of cardiovascular disorders. Novel therapeutic approaches or drug delivery systems for endothelial dysfunctions have had promising beneficial effects in preclinical or clinical levels by affecting the progression of atherosclerotic changes, tumor angiogenesis, and host–immune reactions near tumor environments.
endothelial cells --- oxidative stress --- inflammageing --- endothelial dysfunction --- aldehyde dehydrogenase-2 --- cardiovascular disease --- neurovascular disease --- vascular inflammation --- APE1/Ref-1 --- cardiovascular diseases --- subcellular localization --- serological biomarkers --- atherosclerosis --- aerobic exercise --- PCSK9 --- LOX-1 --- insulin resistance --- macrophage polarity --- serum γ-glutamyltransferase --- essential hypertension --- cardiovascular risk factors --- angiogenesis --- nargenicin A1 --- compound 9 --- VEGF --- VEGFR2 --- HIF-1α --- electronegative low-density lipoprotein --- LDL(–) --- L5 LDL --- oxidized LDL --- oxLDL --- ADMA --- arginine --- arginine paradox --- BH4 --- blood pressure --- COVID-19 --- dietary supplements --- endothelium --- eNOS uncoupling --- heart failure --- hypertension --- L-arginine --- myocardial infarction --- NADPH --- nitric oxide --- peripheral artery disease --- ApoE knockout mouse --- atorvastatin --- VCAM-1 --- galectin-3 --- neutrophil/lymphocyte ratio --- electronegative LDL --- LDL(−) --- lectin-like oxLDL receptor-1 --- dyslipidemia --- chronic venous insufficiency --- prolyl oligopeptidase (POP) --- inflammation --- endothelial disfunction --- lung disease --- endothelial to mesenchymal transition --- pulmonary hypertension --- pulmonary fibrosis --- metformin --- diabetes --- CV risk --- hyperglycemia --- glycated lipoproteins --- glycated LDL --- glycated HDL --- endothelial cell dysfunction --- molecular mechanisms --- epigenetic factors --- therapeutic approaches --- vasoactive factors --- EndoMT --- TGF-β --- epigenetics --- endothelial cell --- glycolysis --- metabolism --- pathological angiogenesis --- tumor microenvironment --- MRI (magnetic resonance imaging) --- high-fat diets --- plaque burden --- low-level laser therapy --- phototherapy --- vascular disease --- healing --- ischemia --- vascular calcification --- chronic kidney disease --- CKD --- uremic toxins --- hyperphosphatemia --- vascular smooth muscle cells --- VSMCs --- macrophages --- n/a --- LDL(-)
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