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Obesity and its co-morbidities, including atherosclerosis, insulin resistance and diabetes, are a world-wide epidemic. Inflammatory immune responses in metabolic tissues have emerged as a universal feature of these metabolic disorders. While initial work highlighted the contribution of macrophages to tissue inflammation and insulin resistance, recent studies demonstrate that cells of the adaptive immune compartment, including T and B lymphocytes and dendritic cells also participate in obesity-induced pathogenesis of these conditions. However, the molecular and cellular pathways by which the innate and adaptive branches of immunity control tissue and systemic metabolism remain poorly understood. To engage in growth and activation, cells need to increase their biomass and replicate their genome. This process presents a substantial bioenergetic challenge: growing and activated cells must increase ATP production and acquire or synthesize raw materials, including lipids, proteins and nucleic acids. To do so, they actively reprogram their intracellular metabolism from catabolic mitochondrial oxidative phosphorylation to glycolysis and other anabolic pathways. This metabolic reprogramming is under the control of specific signal transduction pathways whose underlying molecular mechanisms and relevance to physiology and disease are subject of considerable current interest and under intense study. Recent reports have elucidated the physiological role of metabolic reprogramming in macrophage and T cell activation and differentiation, B- and dendritic cell biology, as well as in the crosstalk of immune cells with endothelial and stem cells. It is also becoming increasingly evident that alterations of metabolic pathways play a major role in the pathogenesis of chronic inflammatory disorders. Due to the scientific distance between immunologists and experts in metabolism (e.g., clinicians and biochemists), however, there has been limited cross-talk between these communities. This collection of articles aims at promoting such cross-talk and accelerating discoveries in the emerging field of immunometabolism.

metabolic syndrome --- Obesity --- Immunometabolism --- TCA cycle --- Glycolysis --- macrophage --- Inflammation --- fatty acid oxidation --- Pentose Phosphate Pathway --- lymphocyte

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Obesity and its co-morbidities, including atherosclerosis, insulin resistance and diabetes, are a world-wide epidemic. Inflammatory immune responses in metabolic tissues have emerged as a universal feature of these metabolic disorders. While initial work highlighted the contribution of macrophages to tissue inflammation and insulin resistance, recent studies demonstrate that cells of the adaptive immune compartment, including T and B lymphocytes and dendritic cells also participate in obesity-induced pathogenesis of these conditions. However, the molecular and cellular pathways by which the innate and adaptive branches of immunity control tissue and systemic metabolism remain poorly understood. To engage in growth and activation, cells need to increase their biomass and replicate their genome. This process presents a substantial bioenergetic challenge: growing and activated cells must increase ATP production and acquire or synthesize raw materials, including lipids, proteins and nucleic acids. To do so, they actively reprogram their intracellular metabolism from catabolic mitochondrial oxidative phosphorylation to glycolysis and other anabolic pathways. This metabolic reprogramming is under the control of specific signal transduction pathways whose underlying molecular mechanisms and relevance to physiology and disease are subject of considerable current interest and under intense study. Recent reports have elucidated the physiological role of metabolic reprogramming in macrophage and T cell activation and differentiation, B- and dendritic cell biology, as well as in the crosstalk of immune cells with endothelial and stem cells. It is also becoming increasingly evident that alterations of metabolic pathways play a major role in the pathogenesis of chronic inflammatory disorders. Due to the scientific distance between immunologists and experts in metabolism (e.g., clinicians and biochemists), however, there has been limited cross-talk between these communities. This collection of articles aims at promoting such cross-talk and accelerating discoveries in the emerging field of immunometabolism.

metabolic syndrome --- Obesity --- Immunometabolism --- TCA cycle --- Glycolysis --- macrophage --- Inflammation --- fatty acid oxidation --- Pentose Phosphate Pathway --- lymphocyte --- metabolic syndrome --- Obesity --- Immunometabolism --- TCA cycle --- Glycolysis --- macrophage --- Inflammation --- fatty acid oxidation --- Pentose Phosphate Pathway --- lymphocyte

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Women and men have probably never been concerned as much by their health as during this COVID-19 pandemic. In this context, lifestyle habits continue to be promoted as allies for daily prevention against diseases. This is valid also for metabolic diseases, among which many affect the liver and are risk factors for aggravating the disease course of COVID-19. In fact, liver diseases are currently a major global health problem. There is a huge range of liver diseases and non-alcoholic fatty liver disease (NAFLD) is the most common chronic hepatic condition, which in some patients progresses to cirrhosis and liver cancer. Currently, substantial efforts are being made to better understand NAFLD, especially, because there is no U.S. Food and Drug Administration (FDA)-approved pharmacological therapy. To explore this disease, metabolomics is the most recently developed omics technology after genomics, transcriptomics, and proteomics. Metabolomics is the large-scale analysis of molecules, known as metabolites that are intermediate or end products of metabolism found within cells, tissues, and biofluids. This technology has a very high potential to identify biomarker candidates for the future development of new therapeutics. The book features articles that address metabolomics technology and its use to document different liver functions and dysfunctions, with a major focus on NAFLD.

Medicine --- nonalcoholic fatty liver disease --- nonalcoholic steatohepatitis --- Fibrosis --- Liver biopsy --- Genomics --- Metabolomics --- Proteomics --- Transcriptomics --- nicotinamide --- NAFLD --- steatosis --- heat stress --- primary mouse hepatocytes --- metabolic profile --- GC-MS --- multivariate statistical analysis --- arachidonic acid --- docosahexaenoic acid --- inflammation --- fibrosis --- lipidomics --- mass spectrometry --- in vitro --- HepaRG --- sodium saccharin --- reference toxicants --- de novo lipogenesis --- carbohydrate response element-binding protein --- ChREBP --- diabetes --- glucose production --- glycogen --- glycolysis --- glycogen storage disease type I --- hexosamine --- pentose phosphate pathway --- acupuncture --- imflammation --- lipid metabolism --- oxidative stress --- metabolomics quantitative profiling --- 1H-NMR spectroscopy --- liver --- bile acids --- metabolomics --- rat plasma --- tandem mass spectrometry --- liquid chromatography --- acetaminophen --- hepatotoxicity --- biomarker --- premalignant --- alcoholic liver disease --- cholestasis --- cirrhosis --- NAFL --- NASH --- standard operating procedures --- urine --- blood --- feces --- tissue --- cells --- liver function --- nonalcoholic fatty liver --- liquid chromatography-mass spectrometry --- nuclear magnetic resonance spectroscopy --- metabolic pathway --- non-alcoholic fatty liver disease --- non-alcoholic steatohepatitis --- transcription factors --- metabolic stress --- lipid homeostasis --- glucose homeostasis

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The book starts with the editors’ preface summarizing the contributions of each of the following thirteen articles dealing with chemical and pharmacological aspects of the molecular modulators of the oxidative stress in regard to various therapeutic approaches in cardiovascular and neurodegenerative diseases, cancer, and diabetes. The seven articles present data from original research studies enlightening the roles and mechanisms of action of small molecular weight compounds (natural and synthetic; ascorbic acid/vitamin C, deferoxamine, N-acetylcysteine, MitoVitE, α-tocopherol, trolox, and ezetimibe) or proteins (SIRT3) in modulation of oxidative stress. In the six review papers, the authors present and discuss the possible therapeutic potential of novel approaches and compounds that are promising and deserve further investigation, in modulation of oxidative stress.

ascorbic acid --- deferoxamine --- N-acetylcysteine --- ischemia/reperfusion --- cardiac fibroblasts --- reactive oxygen species --- photobiomodulation --- reactive oxygen species (ROS) --- nuclear factor kappa-light-chain-enhancer of activated B cells (NF-кB) --- cancer --- diabetes --- wound healing --- glucose --- pentose phosphate pathway --- NADPH --- redox balance --- glycogen --- glycolysis --- stress resistance --- insulin resistance --- immunomodulation --- inflammation --- olive tree --- oxidative stress --- secoirioids --- sirtuin 3 --- high fat diet --- sex differences --- mice --- metabolic stress --- antioxidants --- ADHD --- Nrf2 --- NRF2-KEAP1 --- ROS --- cancer metabolism --- antioxidant --- cancer therapy --- chemoresistance --- radioresistance --- sepsis --- MitoVitE --- mitochondria --- gene expression --- cytokines --- mRNA --- vitamin C --- folic acid --- one-carbon metabolism --- C2C12 cells --- metabolomics --- mass spectrometry --- type 2 diabetes --- dipeptidyl peptidase-4 inhibitors --- biomarkers --- ER stress --- Ezetimibe --- ischemia-reperfusion --- ionizing radiation --- liver --- hydroperoxide --- epigenetics --- miR7/MAFG/Nrf2 axe --- n/a

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Renal cancer is a health problem of major concern worldwide. Although tyrosine kinase inhibitors and immune check-point blockade treatments, alone or in combination, are giving promising results, failures are quite frequent due to intratumor heterogeneity and to the acquisition of drug resistance. The spectrum of renal cell carcinoma subtypes is wide. Up to 70–80% of renal tumors are clear cell renal cell carcinomas, a clinically aggressive tumor subtype linked to VHL gene inactivation. Next in frequency, the papillary renal cell carcinoma category encompasses an intricate puzzle of classic and newly described entities with poorly defined limits, some of them pending definite clarification. Likewise, the chromophobe–oncocytoma duality, the so-called hybrid tumors and oncocytic neoplasms, remain to be well profiled. Finally, a growing list of very uncommon renal tumors linked to specific molecular signatures fulfill the current portrait of renal cell neoplasia. This Special Issue of Cancers regards RCC from very different perspectives, from the intimate basic mechanisms governing this disease to the clinical practice principles of their diagnoses and treatments. The interested reader will have the opportunity to contact with some of the most recent findings and will be updated with excellent reviews.

Renal cell carcinoma. --- Kidneys --- Cancer. --- Adenocarcinoma of kidney --- Clear cell carcinoma --- Grawitz tumor --- Grawitz's tumor --- Hypernephroid carcinoma --- Hypernephroma --- Renal adenocarcinoma --- Renal cell adenocarcinoma --- Cancer --- N-glycomapping --- n/a --- SMAD proteins --- patient survival --- pro-IL-1? --- survival prediction --- inflammation markers --- tumor migration --- prognostic factors --- practical approach --- circular RNAs in a clinico-genomic predictive model --- glycomarkers --- review --- nephrectomy --- uric acid --- VEGF inhibitors --- metabolic reprogramming --- collecting duct carcinoma --- curcumin --- metabolome profiling --- identification of circular RNAs --- IL-2 --- experimental validation of circular RNA --- Raf/MEK/ERK --- HOT --- PI3K/Akt/mTOR --- pentose phosphate pathway --- kidney cancer --- LOT --- mutation --- RCC --- polybromo-1 --- pale cell --- MMP-9 --- gene expression --- recurrence free survival --- chromosomal loss --- IL-1? --- chronic kidney disease --- glutathione transferase omega 2 --- label-free --- glutathione transferase omega 1 --- emerging entity --- copy number alteration --- FOXO3 --- predictive role --- tumor slice culture --- tyrosine kinase inhibitors --- PPP --- ESC --- CDKN1A expression --- metastasis --- PD-L1 --- diagnostic and prognostic markers --- EVI1 --- copy number loss --- RNA sequencing --- NK cells --- glutathione metabolism --- clear cell renal cell carcinoma --- renal cell cancer --- proliferation --- eosinophilic variant --- Xp11 translocation renal cell carcinoma --- prognosis --- invasion --- immune infiltration --- IL4R? --- FISH --- 11) translocation renal cell carcinoma --- tumor microenvironment --- metabolome --- hyperosmolality --- toxicity --- ALK --- drug sensitivity --- t(6 --- copy number analysis --- urine --- genetic association --- polymorphism --- solute carrier proteins --- kidney --- metastatic ccRCC --- molecular genetic features --- recurrence-free survival --- chromophobe renal cell carcinoma --- unclassified renal tumor --- overall survival --- mTOR inhibitors --- mTOR --- JAK2 --- von Hippel–Lindau --- miR-155-5p --- glycoproteomics --- PBRM1 --- miR-133b --- survival --- TFE3 --- TFEB --- oncocytic renal tumor --- immune checkpoint inhibitors --- biomarker --- MMP10 --- TCGA --- ghrelin --- EMT like --- checkpoint inhibitors --- MiT family translocation renal cell carcinoma --- gene signature --- sarcomatoid --- transforming growth factor beta --- clear cell Renal Cell Carcinoma --- tumor adhesion --- renal cancer --- unclassified renal cell carcinoma --- Papillary renal cell carcinoma (pRCC) --- miR-146a-5p --- renal cell --- everolimus --- integrins --- cytoreductive nephrectomy --- immunotherapy --- predictive factors --- immunohistochemistry --- MTA2 --- IL13R?1 --- targeted therapy --- intratumour heterogeneity --- aurora A --- TCA cycle --- AMP-activated protein kinases --- cancer-specific survival --- programmed death-ligand 1 --- efficacy --- renal cell carcinoma --- anaplastic lymphoma kinase rearrangement --- TFEB-amplified renal cell carcinoma --- statins --- cancer immunotherapy --- microRNA --- new entity --- proteome profiling --- von Hippel-Lindau