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Mounting evidence suggests a bidirectional relationship between metabolism and inflammation. Molecular crosstalk between these processes occurs at different levels with the participation of nuclear receptors, including peroxisome proliferator-activated receptors (PPARs). There are three PPAR isotypes, α, β/δ, and γ, which modulate metabolic and inflammatory pathways, making them key for the control of cellular, organ, and systemic processes. PPAR activity is governed by fatty acids and fatty acid derivatives, and by drugs used in clinics (glitazones and fibrates). The study of PPAR action, also modulated by post-translational modifications, has enabled extraordinary advances in the understanding of the multifaceted roles of these receptors in metabolism, energy homeostasis, and inflammation both in health and disease. This Special Issue of IJMS includes a broad range of basic and translational article, both original research and reviews, focused on the latest developments in the regulation of metabolic and/or inflammatory processes by PPARs in all organs and the microbiomes of different vertebrate species.

nuclear receptor --- gene transcription --- inflammation --- molecular docking --- PPARβ/δ --- lung --- pulmonary artery --- GW0742 --- GSK3787 --- docking --- lipopolysaccharide (LPS) --- PPARγ ligand --- coumarin --- fluorescent ligand --- screening --- crystal structure --- PPAR --- atopic dermatitis --- psoriasis --- metabolic reprograming --- glucose --- fatty acids --- mycobacteria --- M. tuberculosis --- M. leprae --- PPARs --- lipid droplets --- metabolic alterations --- hepatic damage --- nuclear factors --- pharmacological targets --- AMPK --- GDF15 --- insulin resistance --- type 2 diabetes mellitus --- peroxisome proliferator-activated receptor gamma (PPARγ) --- real-time PCR --- ELISA --- immunohistochemistry --- signaling pathway --- PPAR gamma --- brain --- neural stem cells --- infection --- neuroinflammation --- HIV --- Zika --- cytomegalovirus --- neurogenesis --- microglia --- liver damage --- toll-like receptor 4 --- P2Y2 receptor --- metabolic syndrome --- resveratrol --- quercetin --- PPARα --- peroxisome --- β-oxidation --- PPRE --- ligand --- coregulator --- micronutrients --- PPARα knockout --- adipose tissue --- browning --- lipid metabolism --- depression --- PPARg --- neuropathology --- corticotropin releasing hormone --- norepinephrine --- subgenual prefrontal cortex --- amygdala --- nucleus accumbens --- common carotid artery occlusion --- electroretinography --- fibroblast growth factor 21 --- pemafibrate --- peroxisome proliferator-activated receptor alpha --- retinal ischemia --- skeletal muscle --- substrate metabolism --- nonalcoholic fatty liver disease (NAFLD) --- sex dimorphism --- lipidomics --- hepatic sex-biased gene expression --- PPARγ --- pulmonary arterial hypertension --- TGFβ --- vascular injury --- proliferation --- kidney fibrosis --- pattern-recognition receptors --- phagocytosis --- nitric oxide synthase --- fenofibrate --- oleoylethanolamide --- palmitoylethanolamide --- cancer --- immunity --- obesity --- diabetes --- miRNA --- DNA methylation --- histone modification --- peroxisome-proliferator-activated receptor --- fatty acid oxidation --- doping control --- regulatory T cells --- exercise --- nuclear receptors --- nutrigenomics --- energy homeostasis --- dairy animals --- non-alcoholic fatty liver disease (NAFLD) --- non-alcoholic steatohepatitis (NASH) --- peroxisome proliferator-activated receptors (PPAR) --- bezafibrate --- fenofibric acid --- peroxisome proliferator-activated receptor --- dual/pan agonist --- X-ray crystallography --- n/a

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This reprint combines recent original manuscripts and reviews covering the multiple functions of peroxisome proliferator-activated receptors in physiology and pathophysiology. Potential applications and limitations of PPAR agonists and antagonists are discussed. All original contributions were published in Cells.

peroxisome-proliferator activated receptors --- tumor angiogenesis --- tumor progression --- metastasis formation --- endothelial cells --- RNA sequencing --- PPARs --- toxicology --- pharmacology --- ligand --- vascular --- coronary artery --- lipidomics --- eicosanoids --- inflammation --- CYP450 --- peroxisome proliferator-activated receptor --- angiogenesis --- proliferation --- metastasis --- immortality --- resistance to cell death --- growth suppressors --- immune system --- cellular metabolism --- PPAR --- nuclear receptors --- addiction --- alcohol --- nicotine --- opioids --- psychostimulants --- animal models --- human studies --- Alzheimer’s --- risk factors --- PPARα --- lipids --- fatty acids --- modulators --- cognition --- sex --- therapy --- hypertrophic adipocytes --- PPARG isoforms --- PPARG splicing --- dominant-negative isoform --- in vitro adipocytes --- adipogenesis --- hypertrophic obesity --- insulin-resistance --- peroxisome proliferator-activated receptors (PPARs) --- synthetic agonists --- non-alcoholic fatty liver disease (NAFLD) --- non-alcoholic steatohepatitis (NASH) --- fibrosis --- Sirtuin1 --- peroxisome proliferator-activated receptor-γ coactivator-1α --- peroxisome proliferator activated receptors --- obesity --- metabolic syndrome --- vitamin B12 --- folate --- fetal programming --- inherited metabolic disorders --- PGC-1α, disease --- kidney --- cancer --- AKI --- CKD --- nephron --- PKD --- cilia --- cystogenesis --- ligands --- Alzheimer’s disease (AD)

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Mounting evidence suggests a bidirectional relationship between metabolism and inflammation. Molecular crosstalk between these processes occurs at different levels with the participation of nuclear receptors, including peroxisome proliferator-activated receptors (PPARs). There are three PPAR isotypes, α, β/δ, and γ, which modulate metabolic and inflammatory pathways, making them key for the control of cellular, organ, and systemic processes. PPAR activity is governed by fatty acids and fatty acid derivatives, and by drugs used in clinics (glitazones and fibrates). The study of PPAR action, also modulated by post-translational modifications, has enabled extraordinary advances in the understanding of the multifaceted roles of these receptors in metabolism, energy homeostasis, and inflammation both in health and disease. This Special Issue of IJMS includes a broad range of basic and translational article, both original research and reviews, focused on the latest developments in the regulation of metabolic and/or inflammatory processes by PPARs in all organs and the microbiomes of different vertebrate species.

Research & information: general --- Biology, life sciences --- Biochemistry --- nuclear receptor --- gene transcription --- inflammation --- molecular docking --- PPARβ/δ --- lung --- pulmonary artery --- GW0742 --- GSK3787 --- docking --- lipopolysaccharide (LPS) --- PPARγ ligand --- coumarin --- fluorescent ligand --- screening --- crystal structure --- PPAR --- atopic dermatitis --- psoriasis --- metabolic reprograming --- glucose --- fatty acids --- mycobacteria --- M. tuberculosis --- M. leprae --- PPARs --- lipid droplets --- metabolic alterations --- hepatic damage --- nuclear factors --- pharmacological targets --- AMPK --- GDF15 --- insulin resistance --- type 2 diabetes mellitus --- peroxisome proliferator-activated receptor gamma (PPARγ) --- real-time PCR --- ELISA --- immunohistochemistry --- signaling pathway --- PPAR gamma --- brain --- neural stem cells --- infection --- neuroinflammation --- HIV --- Zika --- cytomegalovirus --- neurogenesis --- microglia --- liver damage --- toll-like receptor 4 --- P2Y2 receptor --- metabolic syndrome --- resveratrol --- quercetin --- PPARα --- peroxisome --- β-oxidation --- PPRE --- ligand --- coregulator --- micronutrients --- PPARα knockout --- adipose tissue --- browning --- lipid metabolism --- depression --- PPARg --- neuropathology --- corticotropin releasing hormone --- norepinephrine --- subgenual prefrontal cortex --- amygdala --- nucleus accumbens --- common carotid artery occlusion --- electroretinography --- fibroblast growth factor 21 --- pemafibrate --- peroxisome proliferator-activated receptor alpha --- retinal ischemia --- skeletal muscle --- substrate metabolism --- nonalcoholic fatty liver disease (NAFLD) --- sex dimorphism --- lipidomics --- hepatic sex-biased gene expression --- PPARγ --- pulmonary arterial hypertension --- TGFβ --- vascular injury --- proliferation --- kidney fibrosis --- pattern-recognition receptors --- phagocytosis --- nitric oxide synthase --- fenofibrate --- oleoylethanolamide --- palmitoylethanolamide --- cancer --- immunity --- obesity --- diabetes --- miRNA --- DNA methylation --- histone modification --- peroxisome-proliferator-activated receptor --- fatty acid oxidation --- doping control --- regulatory T cells --- exercise --- nuclear receptors --- nutrigenomics --- energy homeostasis --- dairy animals --- non-alcoholic fatty liver disease (NAFLD) --- non-alcoholic steatohepatitis (NASH) --- peroxisome proliferator-activated receptors (PPAR) --- bezafibrate --- fenofibric acid --- peroxisome proliferator-activated receptor --- dual/pan agonist --- X-ray crystallography --- nuclear receptor --- gene transcription --- inflammation --- molecular docking --- PPARβ/δ --- lung --- pulmonary artery --- GW0742 --- GSK3787 --- docking --- lipopolysaccharide (LPS) --- PPARγ ligand --- coumarin --- fluorescent ligand --- screening --- crystal structure --- PPAR --- atopic dermatitis --- psoriasis --- metabolic reprograming --- glucose --- fatty acids --- mycobacteria --- M. tuberculosis --- M. leprae --- PPARs --- lipid droplets --- metabolic alterations --- hepatic damage --- nuclear factors --- pharmacological targets --- AMPK --- GDF15 --- insulin resistance --- type 2 diabetes mellitus --- peroxisome proliferator-activated receptor gamma (PPARγ) --- real-time PCR --- ELISA --- immunohistochemistry --- signaling pathway --- PPAR gamma --- brain --- neural stem cells --- infection --- neuroinflammation --- HIV --- Zika --- cytomegalovirus --- neurogenesis --- microglia --- liver damage --- toll-like receptor 4 --- P2Y2 receptor --- metabolic syndrome --- resveratrol --- quercetin --- PPARα --- peroxisome --- β-oxidation --- PPRE --- ligand --- coregulator --- micronutrients --- PPARα knockout --- adipose tissue --- browning --- lipid metabolism --- depression --- PPARg --- neuropathology --- corticotropin releasing hormone --- norepinephrine --- subgenual prefrontal cortex --- amygdala --- nucleus accumbens --- common carotid artery occlusion --- electroretinography --- fibroblast growth factor 21 --- pemafibrate --- peroxisome proliferator-activated receptor alpha --- retinal ischemia --- skeletal muscle --- substrate metabolism --- nonalcoholic fatty liver disease (NAFLD) --- sex dimorphism --- lipidomics --- hepatic sex-biased gene expression --- PPARγ --- pulmonary arterial hypertension --- TGFβ --- vascular injury --- proliferation --- kidney fibrosis --- pattern-recognition receptors --- phagocytosis --- nitric oxide synthase --- fenofibrate --- oleoylethanolamide --- palmitoylethanolamide --- cancer --- immunity --- obesity --- diabetes --- miRNA --- DNA methylation --- histone modification --- peroxisome-proliferator-activated receptor --- fatty acid oxidation --- doping control --- regulatory T cells --- exercise --- nuclear receptors --- nutrigenomics --- energy homeostasis --- dairy animals --- non-alcoholic fatty liver disease (NAFLD) --- non-alcoholic steatohepatitis (NASH) --- peroxisome proliferator-activated receptors (PPAR) --- bezafibrate --- fenofibric acid --- peroxisome proliferator-activated receptor --- dual/pan agonist --- X-ray crystallography

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This book includes 17 papers published in the Special Issue/Article Collection “New Insights in the Genetics and Genomics of adrenocortical tumors and pheochromocytomas” including an editorial, 10 research papers and six review articles. Adrenal tumors represent a hot topic in contemporary endocrine oncology. Significant advancements in the genetics of genomics of these tumors have been made in recent years, and these articles give a useful and comprehensive overview of these issues. Questions regarding molecular pathogenesis, diagnosis (biomarkers) and even treatment are discussed in the papers written by international leaders of the field. Manuscripts are focused on three main topics: i. primary aldosteronism (the most common cause of secondary endocrine hypertension), ii. adrenocortical cancer and iii. pheochromocytoma/paraganglioma, which are the tumors with the highest heritability in humans. The book is edited by Prof. Peter Igaz (Department of Endocrinology, Faculty of Medicine, Semmelweis University).

Medicine --- pheochromocytoma --- paraganglioma --- genetics --- non-coding RNA --- malignancy --- biomarker --- treatment --- adaptive metabolism --- adrenal gland --- conn adenoma --- fatty acid metabolism --- ferroptosis --- hyperaldosteronism --- metabolic reprogramming --- β-oxidation --- PPARα --- tumor microenvironment --- Next Generation Sequencing --- hereditary cancer --- endocrine tumor syndrome --- KCNJ5 somatic mutation --- pulse wave velocity --- aldosterone-producing adenoma --- adrenalectomy --- propensity score matching --- arterial stiffness --- pheochromocytomas --- paragangliomas --- mutations --- susceptibility genes --- driver mutations --- hereditary --- germline --- somatic --- environment --- variants --- tumor suppressor genes --- metastatic --- RNAseq --- next generation sequencing --- adrenocortical carcinoma --- in silico analysis --- machine learning --- bioinformatic clustering --- biomarker prediction --- aldosterone producing adenoma --- ATP2B3 --- K416-F418delinsN mutation --- primary aldosteronism --- PPGL --- telomeres --- TERT --- ATRX --- NOP10 --- prognostic biomarker --- ALT --- phaeochromocytoma --- cancer --- mitochondrial complex II --- zebrafish --- therapy --- drug discovery --- redox balance pathway --- Vitamin C --- mitotane --- H295 strains --- microRNA --- aldosterone --- circulating --- adrenocortical --- transcriptomics --- epigenetics --- metabolomics --- epidemiology --- genetic analysis --- mortality --- surveillance --- TP53 R337H --- genetic testing --- adrenocortical tumor --- neonatal screening --- screening --- adenoma --- adrenal --- tissue --- artificial intelligence --- neural network --- pheochromocytoma --- paraganglioma --- genetics --- non-coding RNA --- malignancy --- biomarker --- treatment --- adaptive metabolism --- adrenal gland --- conn adenoma --- fatty acid metabolism --- ferroptosis --- hyperaldosteronism --- metabolic reprogramming --- β-oxidation --- PPARα --- tumor microenvironment --- Next Generation Sequencing --- hereditary cancer --- endocrine tumor syndrome --- KCNJ5 somatic mutation --- pulse wave velocity --- aldosterone-producing adenoma --- adrenalectomy --- propensity score matching --- arterial stiffness --- pheochromocytomas --- paragangliomas --- mutations --- susceptibility genes --- driver mutations --- hereditary --- germline --- somatic --- environment --- variants --- tumor suppressor genes --- metastatic --- RNAseq --- next generation sequencing --- adrenocortical carcinoma --- in silico analysis --- machine learning --- bioinformatic clustering --- biomarker prediction --- aldosterone producing adenoma --- ATP2B3 --- K416-F418delinsN mutation --- primary aldosteronism --- PPGL --- telomeres --- TERT --- ATRX --- NOP10 --- prognostic biomarker --- ALT --- phaeochromocytoma --- cancer --- mitochondrial complex II --- zebrafish --- therapy --- drug discovery --- redox balance pathway --- Vitamin C --- mitotane --- H295 strains --- microRNA --- aldosterone --- circulating --- adrenocortical --- transcriptomics --- epigenetics --- metabolomics --- epidemiology --- genetic analysis --- mortality --- surveillance --- TP53 R337H --- genetic testing --- adrenocortical tumor --- neonatal screening --- screening --- adenoma --- adrenal --- tissue --- artificial intelligence --- neural network