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Epigenetics is a new field that explains gene expression at the chromatin structure and organization level. Three principal epigenetic mechanisms are known and hundreds of combinations among them can develop different phenotypic characteristics. DNA methylation, histone modifications and small RNAs have been identified, and their functions are being studied in order to understand the mechanisms of interaction and regulation among the different biological processes in plants. Although, fundamental epigenetic mechanisms in crop plants are beginning to be elucidated, the comprehension of the different epigenetic mechanisms, by which plant gene regulation and phenotype are modified, is a major topic to develop in the near future in order to increase crop productivity. Thus, the importance of epigenetics in improving crop productivity is undoubtedly growing. Current research on epigenetics suggest that DNA methylation, histone modifications and small RNAs are involved in almost every aspect of plant life including agronomically important traits such as flowering time, fruit development, responses to environmental factors, defense response and plant growth. The aim of this Research Topic is to explore the recent advances concerning the role of epigenetics in crop biotechnology, as well as to enhance and promote interactions among high quality researchers from different disciplines such as genetics, cell biology, pathology, microbiology, and evolutionary biology in order to join forces and decipher the epigenetic mechanisms in crop productivity.

crop --- epigenetics --- Biotechnology --- DNA Methylation --- Histone posttranslational modifications --- small non-coding RNAs

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Neurodegenerative diseases (NDs) are a heterogeneous group of disorders affecting the central nervous system. Despite significant differences in their causes, neuropathological abnormalities, and clinical outcomes, some similarities can be found among them, as for example: 1) frequent aggregation and deposition of misfolded proteins, 2) common molecular mechanisms leading to neurodegeneration, and 3) certain overlap in symptoms and clinical features. To date, there is no cure that could stop or delay the progression of these diseases. The advent of advanced gene therapy techniques such as gene silencing and gene editing opened a new avenue for the development of therapeutic strategies for NDs.The discovery of the RNA interference (RNAi) mechanism, in 1998, by Andrew Fire and Craig Mello allowed an important boost to the gene therapy field, providing a potential therapeutic strategy to treat inherited dominant genetic disorders. The use of small RNA sequences to control the expression of disease-causing genes rapidly implemented in the preclinical studies for different diseases. In the field of NDs, several successful studies using this technology proved its potential as a therapeutic option. However, issues like the type of delivery system (non-viral versus viral) or the potential toxicity of the small RNA molecules, made the translation of gene silencing therapeutics to human application very slow and difficult.Recently, a new hope in the gene therapy field emerged with the development of gene editing techniques like TALENs or CRISPR/Cas9 systems. The opportunity of editing or deleting gene sequences drove the scientific community euphoric, with an enormous increase in the number of published studies using this type of techniques. Recently, the first clinical trial using one of these systems was approved in China. For NDs, gene-editing technology also represents an important therapeutic option, and the first preclinical studies are now being published, showing the potential accomplishment for this technology.

Gene silencing --- Gene editing --- Neurodegenerative diseases --- Antisense oligonucleotides --- CRISPR/Cas9 --- Neuroinflammation --- iPS cells --- Long non-coding RNAs --- RNA interference --- Neurodegeneration

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This Special Issue of Cancers (Basel) is mainly dedicated to selecting papers from the talks given during the first Joint Meeting on Lung Cancer (JMLC) between the MD Anderson Cancer Center (Houston, Texas USA) and the Hospital University Federation (HUF) OncoAge (University Côte d’Azur, Nice, France) (Nice, September 2018). The central theme of JMLC is to discuss new advances and exchange ideas regarding lung cancer. Notably, the talks covered different topics on new therapeutic strategies (targeted therapy and immuno-oncology), molecular and cellular biology, biomarkers, and the epidemiology of lung cancer. Special attention was also given to lung cancer in elderly patients. The articles published in this Special Issue covered subjects such as the assessment of new biomarkers and new approaches for the early detection of lung cancer, epidemiological data, and emphasized a place for the newly characterized cellular pathways in lung cancer, which opens room for therapeutic perspectives for lung cancer patients.

cancer --- older adults --- geriatric assessment --- geriatric interventions --- non-small cell lung cancer --- non-smoker --- tumor microenvironment --- targeted treatment --- lung cancer --- artificial intelligence --- screening --- lncRNA --- MALAT1 --- metastasis --- bioinformatics --- integrated approaches --- lung cancer --- rational therapy --- immune profiling --- cancer tissues --- multiplexed methodologies --- image analysis --- spatial analysis --- aging --- cancer --- optimization --- research --- education --- elderly --- well-being --- circulating tumor cells --- liquid biopsy --- lung cancer --- personal medicine --- techniques --- xenograft --- multiplexed --- brightfield --- chromogenic --- fluorescence --- molecular --- immune profiling --- immune-oncology --- digital --- lung cancer --- lung adenocarcinoma --- macrophage --- immunotherapy --- interleukin-1? and immunometabolism --- lung cancer --- EGFR mutations --- EGFR TKIs --- non-coding RNAs --- microRNAs --- long non-coding RNAs --- hormones --- hormone-like action --- non-small cell lung cancer --- immunotherapy --- PD-1/PD-L1 checkpoint blockade --- CD8 T Cells --- immune blockade --- NSCLC --- reversal of EMT --- tumor microenvironment --- tumor plasticity --- TNBC

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Acute kidney injury (AKI) is still associated with high morbidity and mortality incidence rates, and also bears an elevated risk of subsequent chronic kidney disease. Although the kidney has a remarkable capacity for regeneration after injury and may recover completely depending on the type of renal lesions, the options for clinical intervention are restricted to fluid management and extracorporeal kidney support. The development of novel therapies to prevent AKI, to improve renal regeneration capacity after AKI, and to preserve renal function is urgently needed. The Special Issue covers research articles that investigated the molecular mechanisms of inflammation and injury during different renal pathologies, renal regeneration, diagnostics using new biomarkers, and the effects of different stimuli like medication or bacterial components on isolated renal cells or in vivo models. The Special Issue contains important reviews that consider the current knowledge of cell death and regeneration, inflammation, and the molecular mechanisms of kidney diseases. In addition, the potential of cell-based therapy approaches that use mesenchymal stromal/stem cells or their derivates is summarized. This edition is complemented by reviews that deal with the current data situation on other specific topics like diabetes and diabetic nephropathy or new therapeutic targets.

kidney injury --- alport syndrome --- modifier gene --- nephrin --- podocin --- glomerular basement membrane --- slit diaphragm --- focal segmental glomerulosclerosis --- inflammatory bowel disease (IBD) --- DSS-colitis --- glomerular filtration barrier (GFB) --- type IV collagen --- type I collagen --- type V collagen --- genotype --- IL-18 --- polymorphism --- renal cell carcinoma --- Taiwan --- mesenchymal stem cells --- acute and chronic kidney disease --- exosome --- natural products --- non-coding RNAs --- microRNAs --- long non-coding RNAs --- renal fibrosis --- biomarkers --- therapeutics targets --- rhabdomyolysis --- pigment nephropathy --- haem --- NLRP3 inflammasome --- acute kidney injury --- hypertension --- kidney --- molecular signaling --- hematuria --- inflammation --- oxidative stress --- tubular injury --- AKI --- chronic kidney disease (CKD) --- mesenchymal stromal cells --- extracellular vesicles --- acute kidney injury --- modified-MSCs --- microRNA --- mesenchymal stem cell --- mesodermal stem cell --- renal ischemia-reperfusion --- inflammation --- kidney transplantation --- microRNA --- extracellular vesicles --- exosomes --- B-cell attracting chemokine --- CXCL13 --- kidney transplantation --- allograft rejection --- T cell-mediated rejection --- diabetic nephropathy --- lysophosphatidic acid --- lysophosphatidic acid receptor --- chronic kidney injury --- kidney proximal tubule --- acute kidney failure --- signal transduction --- transcription --- CREB Regulated Transcriptional Coactivators (CRTC) --- cAMP Regulatory Element Binding Protein (CREB) --- Salt Inducible Kinase (SIK) --- Class IIa Histone Deacetylases (HDAC) --- lncRNA --- long non-coding RNA --- miRNA --- kidney --- glomerulus --- podocyte --- acute kidney injury --- AKI --- diabetic nephropathy --- diabetic kidney disease --- diabetic nephropathy --- inflammation --- signaling cascade --- ischemia-reperfusion --- acute kidney injury --- stem cell --- conditioned medium --- inflammation --- apoptosis --- necrosis --- regulated necrosis --- kidney injury --- tubular injury --- glomerular injury --- polyunsaturated fatty acids --- omega-3 fatty acid --- inflammatory maker --- C-reactive protein --- interleukin-6 --- LPS-binding protein --- fibrosis --- pericyte --- myofibroblast --- endotoxemia-induced oliguric kidney injury --- arachidonic acid --- cyclooxygenase --- lipoxygenase --- cytochrome P450 --- kidney inflammation --- therapeutic target --- obese kidney fibrosis --- endotoxemia --- ROS --- cPLA2 and COX-2 --- IgA nephropathy --- KIT assay --- KIT-IgA score --- noninvasive --- diagnostics --- prediction --- diabetic kidney diseases --- xanthine oxidase --- glomerular damage --- acute kidney injury --- chronic kidney disease --- renal progenitors --- polyploidization --- diabetic nephropathy --- diabetes mellitus --- GLP-1 receptor agonists --- SGLT2 inhibitors --- molecular mechanisms --- chemerin --- CmklR1 --- 2-kidney-1-clip --- 2k1c --- Thy1.1 nephritis --- renovascular hypertension --- renal inflammation --- renal injury --- renal fibrosis --- inflammation --- ischemia/reperfusion injury --- Farnesiferol B --- Nuclear Factor kappa-light-chain-enhancer of activated B cells (NF-?B) --- G-protein-coupled bile acid receptor (TGR5) --- renal stem cells --- differentiation --- scattered tubular cells --- papilla --- niches --- renal tubular cells --- epithelial cells --- proximal tubule --- cytotoxicity --- injury --- inflammation --- empagliflozin --- dapagliflozin --- kidney --- n/a