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The Epithelial-to-Mesenchymal Transition (EMT) in Cancer

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ISBN: 9783038427933 9783038427940 Year: Pages: VI, 254 Language: English
Publisher: MDPI - Multidisciplinary Digital Publishing Institute
Subject: Biology
Added to DOAB on : 2018-04-27 16:09:54
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Abstract

The epithelial-to-mesenchymal transition (EMT) is a highly dynamic process with multiple transitional states, by which epithelial cells can convert into a mesenchymal phenotype. This process involves loss of cellular adhesion and cellular polarity, and an improvement in migratory and invasive properties. It occurs during normal embryonic development, tissue regeneration, organ fibrosis, and wound healing. It is also involved in tumor progression with metastatic expansion, and plays a major role in resistance to cancer treatment. In cancers, EMT inducers are hypoxia, cytokines and growth factors secreted by the tumor microenvironment, stroma crosstalk, metabolic changes, innate and adaptive immune responses, and treatment with antitumor drugs. Switch in gene expression from epithelial to mesenchymal phenotype is triggered by complex regulatory networks involving transcriptional control, non-coding RNAs, chromatin remodeling and epigenetic modifications, alternative splicing, post-translational regulation, protein stability and subcellular localization. Reversion of EMT, the mesenchymal-to-epithelial transition (MET), affects circulating cancer cells when they reach a desirable metastatic niche to develop secondary tumors. More knowledge and control of EMT to MET is necessary and will be beneficial for patients for cancer treatment. This current Special Issue entitled “Epithelial to Mesenchymal Transition in Cancer” will address these questions.

Kidney Inflammation, Injury and Regeneration

Authors: --- ---
ISBN: 9783039285389 / 9783039285396 Year: Pages: 496 DOI: 10.3390/books978-3-03928-539-6 Language: eng
Publisher: MDPI - Multidisciplinary Digital Publishing Institute
Subject: Medicine (General) --- Internal medicine
Added to DOAB on : 2020-06-09 16:38:57
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Abstract

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.

Keywords

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

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