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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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Dear Colleagues, The brain is vulnerable to injury. Following injury in the brain, apoptosis or necrosis may occur easily, leading to various functional disabilities. Neuronal death is associated with a number of neurological disorders including hypoxic ischemia, epileptic seizures, and neurodegenerative diseases. The brain subjected to injury is regarded to be responsible for the alterations in neurotransmission processes, resulting in functional changes. Oxidative stress produced by reactive oxygen species has been shown to be related to the death of neurons in traumatic injury, stroke, and neurodegenerative diseases. Therefore, scavenging or decreasing free radicals may be crucial for preventing neural tissues from harmful adversities in the brain. Neurotrophic factors, bioactive compounds, dietary nutrients, or cell engineering may ameliorate the pathological processes related to neuronal death or neurodegeneration and appear beneficial for improving neuroprotection. As a result of neuronal death or neuroprotection, the brain undergoes activity-dependent long-lasting changes in synaptic transmission, which is also known as functional plasticity. Neuroprotection implying the rescue from neuronal death is now becoming one of global health concerns. This Special Issue attempts to explore the recent advances in neuroprotection related to the brain. This Special Issue welcomes original research or review papers demonstrating the mechanisms of neuroprotection against brain injury using in vivo or in vitro models of animals as well as in clinical settings. The issues in a paper should be supported by sufficient data or evidence. Prof. Bae Hwan Lee Guest Editor

global cerebral ischemia --- amiloride --- sodium–hydrogen exchanger-1 --- zinc --- neuronal death --- neuroprotection --- neurodegenerative disorder --- choline acetyltransferase (ChAT) --- trimethyltin (TMT) --- bean phosphatidylserine (Bean-PS) --- brain-derived neurotrophic factor --- moderate hypoxia --- physical exercise --- psychomotor function --- reaction time --- cortisol --- catecholamines --- nitrite --- endotheline-1 --- lactate --- pyridoxine deficiency --- ischemia --- gerbil --- homocysteine --- cell death --- glia --- neurogenesis --- N-acetyl-l-cysteine --- transient receptor potential melastatin 2 --- neurodegeneration --- Alzheimer’s disease --- metabolic disease --- adiponectin --- insulin --- antioxidants --- stroke --- preventive gene therapy --- adenoviral vector --- VEGF --- GDNF --- NCAM --- human umbilical cord blood mononuclear cells --- antioxidant --- brain --- neurodegenerative disease --- oxidative stress --- PGC-1α --- vascular endothelial growth factor --- vascular endothelial growth factor receptor 2 --- PI3K/AKT --- MEK/ERK --- status epilepticus --- hippocampus --- middle cerebral artery occlusion --- reperfusion injury --- lipid emulsion --- excitotoxicity --- apoptosis --- GPR4 receptor --- MPP+ --- Parkinson’s disease --- CRISPR/cas9 --- ischemic stroke --- blood brain barrier --- nanoparticle-based drug delivery --- brain targeting --- BDNF --- miRNAs --- synaptic plasticity --- depression --- glioblastoma --- astrocytes --- astrocytic networks --- connexin 43 --- calcium activity --- neural injury --- nimodipine --- subarachnoid haemorrhage --- acid-sensing ion channels --- oxygen-glucose deprivation --- liver growth factor --- inflammation --- microglia --- Tg2576 transgenic mice --- amyloid-beta --- oculomotor system --- trophic factors --- motoneurons --- axotomy --- amyotrophic lateral sclerosis --- electroneutral transport --- cation-chloride cotransporters --- KCCs --- NKCCs --- WNK-SPAK/OSR1 --- ascorbic acid --- aging --- organotypic hippocampal slice culture --- n/a --- sodium-hydrogen exchanger-1 --- Alzheimer's disease --- Parkinson's disease