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Hypoxia in Kidney Disease

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889456178 Year: Pages: 143 DOI: 10.3389/978-2-88945-617-8 Language: English
Publisher: Frontiers Media SA
Subject: Science (General) --- Physiology
Added to DOAB on : 2019-01-23 14:53:43
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Abstract

Kidney disease is a complex health problem, often coinciding with cardiovascular pathology (e.g. hypertension) and metabolic disturbances (e.g. obesity and diabetes). It is also a disturbingly fast growing global public health problem, e.g. chronic kidney disease affects an estimated ~9-16% of the population. Besides the public health issues this results in a large economic burden as kidney diseases contributes disproportionally to about a quarter of total health care costs. Experimental and clinical data solidly support the view that kidney tissue hypoxia plays a critical and intricate role during the genesis and progression of both chronic and acute kidney diseases. This research field is currently at the very beginning of integrating pre-clinical with clinical research in which hypoxia related mechanism are quantified by non-invasive imaging. In combination with the fact that some key questions remain unanswered, this offers exciting new research perspectives that are waiting to be explored. With this Research Topic we aim to discuss and find answers to the following research question: 1) What are the temporal relationships between hypoxia and kidney disease? 2) Can we demonstration causation between hypoxia and kidney disease? 3) Can renal hypoxia be considered as a treatment target in kidney disease? 4) Can hypoxia (e.g. in the urine) be considered a biomarker of kidney disease? 5) Does hypoxia ramp-up sympathetic activity? 6) Does hypoxia trigger inflammation? 7) Is hypoxia caused by changes in sodium reabsorption and/or mitochondrial function? 8) Which molecular mechanisms are involved in hypoxia in kidney disease? 9) Which gene expressions change due to hypoxia in kidney disease? 10) Can we generate new and translational insights using non-invasive imaging technologies? Our overall aim is identify the mediators/controllers of hypoxia in kidney disease. If we understand more about the sequence of events leading to hypoxia, its regulation and consequences in renal disease, we might be able to have a major impact in clinical practice. I.e. more accurate and earlier diagnosis, novel treatment targets, and novel therapies.

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

Major Histocompatibility Complex (MHC) in Health and Disease

Authors: --- ---
ISBN: 9783039280728 9783039280735 Year: Pages: 375 DOI: 10.3390/books978-3-03928-073-5 Language: English
Publisher: MDPI - Multidisciplinary Digital Publishing Institute
Subject: Science (General) --- Biology
Added to DOAB on : 2020-04-07 23:07:08
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Abstract

The major histocompatibility complex (MHC) is a highly polymorphic and diverse multigene locus in all jawed vertebrate species that has an integral role in adaptive/innate immune systems, transplantation, and infectious and autoimmune diseases. The MHC supra-locus in mammalian vertebrates is usually partitioned into three distinct regions, known as classes I, II, and III, which, to varying extents, can be found conserved in nonmammalian jawed vertebrates, such as bony fish, amphibians, and bird lineages. The MHC gene region is characterized particularly by the expression of class I and class II glycoproteins that bind peptides derived from intracellular or extracellular antigens to circulating T-cells. While this expressed antigenic specificity remains the predominant interest with respect to MHC function and polymorphism in a population, a broader concept has emerged that examines the MHC as a multifunctional polymorphic controller that facilitates and regulates genome diversity with a much greater array of functions and effects than just MHC-restricted antigen recognition. This volume of 19 reprints presented by various experts and collected from the Special Issue of Cells on “MHC in Health and Disease” covers a broad range of topics on the genomic diversity of the MHC regulatory system in various vertebrate species, including MHC class I, II, and III genes; innate and adaptive immunity; neurology; transplantation; haplotypes; infectious and autoimmune diseases; fecundity; conservation; allelic lineages; and evolution. Taken together, these articles demonstrate the immense complexity and diversity of the MHC structure and function within and between different vertebrate species.

Keywords

MHC-I- and MHC-II-dependent inter-individual recognition --- MHC-II-associated sperm-egg recognition --- MHC-I-based mother-fetus recognition --- giant panda --- long-fragment super haplotype --- MHC --- genetic drift --- haplotype --- crested ibis --- founder effect --- bottleneck --- conservation genetics --- selection --- fish --- MHC --- polymorphism --- disease resistance --- quantitative trait loci (QTL) studies --- evolution --- HCP5 --- lncRNA --- MHC --- HLA --- human endogenous retrovirus (HERV) --- cancer --- autoimmune diseases --- competing endogenous RNA (ceRNA) --- human immunodeficiency virus (HIV) --- human papillomavirus (HPV) --- astrogliosis --- PNS/CNS interface --- microglial reaction --- synaptic covering --- ?2m knockout mice --- HLA-B27 --- viral peptides --- computational analysis --- ankylosing spondylitis --- KIR --- KIR–HLA pairs --- ethnic populations in China --- molecular dynamics simulation --- major histocompatibility complex --- antigen --- T-cell receptor --- domain movements --- autoimmunity --- risk genes --- expression --- regulation --- swine leukocyte antigen --- reproductive performance --- production trait --- haplotype --- micro-mini-pigs --- disease association --- haplotype --- HLA polymorphism --- major histocompatibility complex (MHC) --- pedigree --- phase --- protocol --- single nucleotide polymorphism (SNP) --- T1DGC --- type 1 diabetes (T1D) --- BK virus --- polyomavirus --- nephropathy --- human leukocyte antigen-E --- kidney transplantation --- MHC --- ancestral haplotype --- autoimmune disease --- cynomolgus macaque --- Macaca fascicularis --- MHC polymorphism --- experimental medicine --- nonhuman primate models --- DXO --- DOM3Z --- NELF-E --- RD --- SKIV2L --- SKI2W --- STK19 --- RP1 --- NSDK --- RLR --- miR1236 --- SVA --- RNA quality control --- 5??3? RNA decay --- 3??5? mRNA turnover --- antiviral immunity --- interferon ? --- promoter-proximal transcriptional pause --- exosomes --- nuclear kinase --- hepatocellular carcinoma --- Ski complex --- trichohepatoenteric syndrome --- melanoma --- major histocompatibility complex --- MHC --- evolution --- nonclassical --- fish --- MHC genes --- birds --- disease resistance --- orthology --- life history --- gene duplication --- long-read sequencing --- high-throughput sequencing --- concerted evolution --- ecology --- MHC --- major histocompatibility complex --- Old World camels --- camels --- dromedary --- Bactrian camel --- SNP --- n/a

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