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Mitogen-activated protein kinases (MAPK) are a large family of enzymes that function as signal transducers to regulate a diverse range of physiological responses. However, signaling via extracellular signal-regulated kinase (ERK), c-Jun amino terminal kinase (JNK), and p38 MAPK also underpin many disease processes. This Special Issue provides new insights into how MAPK signaling contributes to specific pathological processes across a range of conditions, including disorders of lung development, type 2 diabetes, proliferative skin diseases, cardiovascular diseases, and neurological diseases.

Rabdosia inflexa --- inflammation --- gastric ulcer --- cytokines --- MAPK --- NF-κB --- extracellular signal-regulated kinases 1/2 --- hyperoxia --- bronchopulmonary dysplasia --- HPAECs --- angiogenesis --- cell cycle --- SIRT1 --- oxidative stress --- psoriasis --- antimicrobial peptide --- cecropin A --- tight junction protein --- MEK/ERK signaling --- porcine intestinal epithelial cell --- extracellular signal-regulated kinase 5 (ERK5) --- Kv4.2 --- PC12 cells --- infantile myofibromatosis --- receptor tyrosine kinases --- platelet-derived growth factor receptor --- protein kinase inhibitors --- sunitinib --- erlotinib --- FR180204 --- U0126 --- targeted therapy --- apoptosis --- ERK1/2 --- JNKs --- mitochondrial dysfunction --- neurodegeneration --- neuro-inflammation --- p38 MAPKs --- Parkinson’s disease --- mitogen-activated protein kinases (MAPKs) --- MAPK kinetics --- osteoclast differentiation --- bone remodeling --- DAPK --- ERK --- p38 --- JNK --- mitogen-activated protein kinase pathway (MAPK pathway) --- protein tyrosine phosphatase interacting protein 51 (PTPIP51) --- protein-protein interaction (PPI) --- cancer signaling --- SR --- CR --- Compatibility --- T2DM --- metabolic profiling --- MAPK/PI3K/Akt signaling pathway --- reactive oxygen species --- PTPN6 --- SRC --- DOK4 --- MKK4 --- MKK7 --- p53 --- DUSP1 --- SIRT2 --- atherosclerosis --- aortic valve sclerosis --- aortic valve stenosis --- naphthalimide-metal complex conjugates --- N-heterocyclic carbene --- mitochondria --- ROS --- p38 MAPK --- cancer --- FGF-induced signaling --- FRS2 --- phosphorylation --- downregulation --- n/a --- Parkinson's disease

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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

Research & information: general --- 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

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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