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Kidney International, ISSN 0085-2538, 01/2018, Volume 93, Issue 1, pp. 147 - 158
We examined activin receptor type IIA (ActRIIA) activation in chronic kidney disease (CKD) by signal analysis and inhibition in mice with Alport syndrome using... 
cardiovascular disease | chronic kidney disease | bone | fibrosis | mineral metabolism | vascular calcification | TGF-BETA | CARDIOVASCULAR EVENTS | RENAL FIBROSIS | ARTERIAL CALCIFICATION | BONE MORPHOGENETIC PROTEIN-7 | GROWTH-FACTOR 23 | UROLOGY & NEPHROLOGY | SMOOTH-MUSCLE-CELLS | LINKED ALPORT-SYNDROME | OSTEOCLAST DIFFERENTIATION | ATHEROSCLEROTIC LESION | Kidney - pathology | Recombinant Fusion Proteins - pharmacology | Blood Vessels - metabolism | Chronic Kidney Disease-Mineral and Bone Disorder - metabolism | Core Binding Factor Alpha 1 Subunit - metabolism | Chronic Kidney Disease-Mineral and Bone Disorder - genetics | Vascular Calcification - metabolism | Kidney - metabolism | Bone Resorption - genetics | Bone and Bones - metabolism | Myocardium - metabolism | Renal Insufficiency, Chronic - genetics | Bone Resorption - metabolism | Disease Models, Animal | Bone Resorption - physiopathology | Glomerular Filtration Rate | Signal Transduction | Smad2 Protein - metabolism | Cardiomegaly - physiopathology | Nephritis, Hereditary - genetics | Renal Insufficiency, Chronic - physiopathology | Mice, Knockout | Renal Insufficiency, Chronic - prevention & control | Cardiomegaly - prevention & control | Nephritis, Hereditary - metabolism | Collagen Type IV - deficiency | Activin Receptors, Type II - genetics | Fibrosis | Sp7 Transcription Factor - metabolism | Collagen Type IV - genetics | Cardiomegaly - metabolism | Activin Receptors, Type II - metabolism | Bone and Bones - pathology | Phosphorylation | Vascular Remodeling | Blood Vessels - pathology | Vascular Calcification - genetics | Actins - metabolism | Chronic Kidney Disease-Mineral and Bone Disorder - physiopathology | Activin Receptors, Type II - antagonists & inhibitors | Blood Vessels - physiopathology | Renal Insufficiency, Chronic - metabolism | Ventricular Remodeling | Chronic Kidney Disease-Mineral and Bone Disorder - prevention & control | Muscle Proteins - metabolism | Vascular Calcification - physiopathology | Microfilament Proteins - metabolism | Nephritis, Hereditary - physiopathology | Kidney - physiopathology | Vascular Calcification - prevention & control | Myocardium - pathology | Bone Resorption - prevention & control | Bone and Bones - physiopathology | Animals | Nephritis, Hereditary - drug therapy | Cardiomegaly - genetics | Bone Remodeling | Chronic kidney disease
Journal Article
Kidney International, ISSN 0085-2538, 06/2014, Volume 85, Issue 6, pp. 1318 - 1329
Hydrogen sulfide has recently been found decreased in chronic kidney disease. Here we determined the effect and underlying mechanisms of hydrogen sulfide on a... 
chronic inflammation | cell signaling | chronic renal disease | PATHWAYS | MECHANISMS | DAMAGE | EPITHELIAL-CELLS | INFLAMMATION | TUBULOINTERSTITIAL FIBROSIS | UROLOGY & NEPHROLOGY | GENERATION | CHRONIC KIDNEY-DISEASE | URETERAL OBSTRUCTION | ISCHEMIA/REPERFUSION | Hydrogen Sulfide - metabolism | Ureteral Obstruction - complications | Phosphorylation | Kidney - pathology | DNA Replication - drug effects | Actins - metabolism | Extracellular Matrix - metabolism | Cystathionine gamma-Lyase - metabolism | Male | Ureteral Obstruction - metabolism | Dose-Response Relationship, Drug | Kidney - metabolism | Nephritis, Interstitial - metabolism | Nephritis, Interstitial - pathology | Time Factors | Nephritis, Interstitial - prevention & control | Inflammation Mediators - metabolism | Sulfides - metabolism | Ureteral Obstruction - drug therapy | Cytoprotection | Disease Models, Animal | Kidney Diseases - metabolism | Sulfides - pharmacology | Cell Line | Hydrogen Sulfide - pharmacology | Kidney - drug effects | Cytokines - metabolism | Kidney Diseases - pathology | Kidney Diseases - prevention & control | Extracellular Matrix - drug effects | Cystathionine beta-Synthase - metabolism | Rats, Sprague-Dawley | Collagen - metabolism | Macrophages - metabolism | Animals | Signal Transduction - drug effects | Ureteral Obstruction - pathology | Fibrosis | Macrophages - drug effects | Cell Proliferation - drug effects | Kidney Diseases - etiology | Mitogen-Activated Protein Kinases - metabolism | Basic Research
Journal Article
Kidney International, ISSN 0085-2538, 02/2009, Volume 75, Issue 3, pp. 285 - 294
Urinary neutrophil gelatinase-associated lipocalin (Ngal or lipocalin 2) is a very early and sensitive biomarker of kidney injury. Here we determined the... 
albuminuria | acute renal failure | obstructive nephropathy | diabetic nephropathy | nephrotic syndrome | Diabetic nephropathy | Obstructive nephropathy | Nephrotic syndrome | Albuminuria | Acute renal failure | NGAL | ACUTE KIDNEY INJURY | MOUSE | DIABETIC-NEPHROPATHY | IRON | TISSUE GROWTH-FACTOR | CARDIAC-SURGERY | INSULIN-RESISTANCE | UROLOGY & NEPHROLOGY | ALBUMIN | RENAL INJURY | Acute-Phase Proteins - urine | Biomarkers - urine | Nephrotic Syndrome - urine | Nephritis, Interstitial - urine | Angiotensin II Type 1 Receptor Blockers - therapeutic use | Humans | Proto-Oncogene Proteins - urine | Nephrotic Syndrome - metabolism | Lipocalins - urine | Loop of Henle - metabolism | Ureteral Obstruction - metabolism | RNA, Messenger - metabolism | Nephritis, Interstitial - metabolism | Time Factors | Sensitivity and Specificity | Kidney Glomerulus - metabolism | Diabetes Mellitus, Experimental - metabolism | Benzimidazoles - therapeutic use | Disease Models, Animal | Diabetic Nephropathies - urine | Lipocalins - metabolism | Proto-Oncogene Proteins - metabolism | Kidney Tubules, Proximal - cytology | Acute-Phase Proteins - metabolism | Albumins - metabolism | Diabetic Nephropathies - metabolism | Mice, Inbred C57BL | Mice, Transgenic | Animals | Lipocalin-2 | Kidney Tubules, Proximal - metabolism | Tetrazoles - therapeutic use | Mice | Acute Kidney Injury - metabolism | Nephrons - metabolism
Journal Article
Journal Article
Biochemical and Biophysical Research Communications, ISSN 0006-291X, 04/2017, Volume 486, Issue 2, pp. 451 - 457
Klotho, an antiaging protein, can extend the lifespan and modulate cellular responses to inflammation and oxidative stress which can ameliorate chronic kidney... 
Cyclosporine A | PDLIM2 | Nephropathy | Klotho | NF-kB p65 | GLOMERULONEPHRITIS | OXIDATIVE STRESS | ACTIVATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | MODEL | BIOPHYSICS | DISEASE | MICE | KIDNEY | ANTIAGING GENE | RENAL INJURY | EXPRESSION | Tumor Necrosis Factor-alpha - metabolism | RNA, Small Interfering - genetics | Epithelial Cells - metabolism | Interleukin-12 - genetics | Blood Urea Nitrogen | Epithelial Cells - drug effects | Tumor Necrosis Factor-alpha - genetics | Glucuronidase - metabolism | Male | Cyclosporine | LIM Domain Proteins - metabolism | Transcription Factor RelA - genetics | Nephritis, Interstitial - metabolism | Nephritis, Interstitial - pathology | Adaptor Proteins, Signal Transducing - antagonists & inhibitors | Adenoviridae - genetics | Chemokine CCL2 - metabolism | Interleukin-6 - metabolism | Nephritis, Interstitial - chemically induced | Cell Line | Kidney Tubules, Proximal - pathology | Genetic Vectors - chemistry | Interleukin-6 - genetics | Macrophages - pathology | Signal Transduction | LIM Domain Proteins - antagonists & inhibitors | Gene Expression Regulation | Genetic Vectors - metabolism | Chemokine CCL2 - genetics | Epithelial Cells - pathology | Interleukin-12 - metabolism | Mice, Inbred ICR | Macrophages - metabolism | Animals | Glucuronidase - genetics | Nephritis, Interstitial - genetics | Nitric Oxide Synthase Type II - genetics | Transcription Factor RelA - metabolism | Adaptor Proteins, Signal Transducing - genetics | Kidney Tubules, Proximal - metabolism | Creatinine - blood | LIM Domain Proteins - genetics | Mice | Adenoviridae - metabolism | Glucuronidase - pharmacology | Adaptor Proteins, Signal Transducing - metabolism | Nitric Oxide Synthase Type II - metabolism | RNA, Small Interfering - metabolism | Medical research | Urea | Medical colleges | Chronic kidney failure | RNA | Luciferase | Medicine, Experimental
Journal Article
The Journal of Pathology, ISSN 0022-3417, 06/2012, Volume 227, Issue 2, pp. 175 - 188
TGF‐β1 binds receptor II (TβRII) to exert its biological activities but its functional importance in kidney diseases remains largely unclear. In the present... 
Smad | renal fibrosis | TGF‐β receptor II | renal inflammation | TGF-β receptor II | KIDNEY-DISEASE | CRESCENTIC GLOMERULONEPHRITIS | TGF-ss receptor II | PATHOLOGY | SMAD7 | PROTECTS | GROWTH-FACTOR-BETA | UNILATERAL URETERAL OBSTRUCTION | ONCOLOGY | LATENT TGF-BETA-1 | SIGNALING MECHANISM | GENE-TRANSFER | TRANSGENIC MICE | Protein-Serine-Threonine Kinases - deficiency | Ureteral Obstruction - complications | Receptors, Transforming Growth Factor beta - genetics | Kidney - pathology | Nephritis - genetics | Humans | Transforming Growth Factor beta1 - metabolism | Kidney - immunology | NF-kappa B - metabolism | Nephritis - pathology | Smad3 Protein - metabolism | Ureteral Obstruction - metabolism | Extracellular Signal-Regulated MAP Kinases - metabolism | Kidney - metabolism | Transfection | Time Factors | Interleukin-1beta - metabolism | Inflammation Mediators - metabolism | p38 Mitogen-Activated Protein Kinases - metabolism | Kidney Tubules - pathology | Kidney Tubules - metabolism | Protein-Serine-Threonine Kinases - metabolism | Disease Models, Animal | Fibroblasts - metabolism | Signal Transduction | Cells, Cultured | Protein-Serine-Threonine Kinases - genetics | Nephritis - etiology | Fibroblasts - pathology | Mice, Knockout | Animals | Receptors, Transforming Growth Factor beta - metabolism | Ureteral Obstruction - pathology | Fibrosis | Nephritis - metabolism | Mice | Receptors, Transforming Growth Factor beta - deficiency
Journal Article
Science, ISSN 0036-8075, 2/2005, Volume 307, Issue 5712, pp. 1107 - 1110
Prions typically accumulate in nervous and lymphoid tissues. Because proinflammatory cytokines and immune cells are required for lymphoid prion replication, we... 
Spleen | Nephritis | Kidneys | B lymphocytes | Transgenic animals | Prions | Liver | Prion diseases | Reports | Inflammation | Pancreas | PATHOGENESIS | SCRAPIE | PROTEIN | REPLICATION | NONOBESE DIABETIC MICE | MULTIDISCIPLINARY SCIENCES | FOLLICULAR DENDRITIC CELLS | LYMPHOID NEOGENESIS | CREUTZFELDT-JAKOB-DISEASE | EXPRESSION | LYMPHOTOXIN | Inflammation - pathology | Liver - pathology | Spleen - immunology | Kidney - pathology | PrPSc Proteins - analysis | Kidney - immunology | Chemokine CCL21 | Lymphotoxin-alpha - metabolism | Nephritis - pathology | PrPSc Proteins - metabolism | Tissue Distribution | Inflammation - metabolism | Kidney - metabolism | Liver - immunology | Lymphocytes - immunology | Nephritis - immunology | Islets of Langerhans - metabolism | Hepatitis - metabolism | Lymphotoxin-beta | Pancreatitis - immunology | Scrapie - immunology | Membrane Proteins - metabolism | PrPC Proteins - metabolism | Liver - metabolism | Mice, Inbred C57BL | Hepatitis - pathology | Islets of Langerhans - immunology | Pancreas - pathology | Mice, Transgenic | Inflammation - immunology | Scrapie - metabolism | Pancreas - metabolism | Pancreas - immunology | Animals | Spleen - metabolism | Scrapie - pathology | Hepatitis - immunology | Nephritis - metabolism | Pancreatitis - pathology | Mice | Pancreatitis - metabolism | Chemokines, CC - metabolism | Care and treatment | Research | Lymphoid tissue | Observations | Bovine spongiform encephalopathy | Lymphocyte receptors | Pathology | Rodents
Journal Article
Kidney International, ISSN 0085-2538, 03/2017, Volume 91, Issue 3, pp. 587 - 602
Mincle (macrophage-inducible C-type lectin, Clec4e) is a transmembrane pattern recognition receptor involving the innate immunity, but its role in kidney... 
inflammation | M1 macrophage | macrophage-inducible C-type lectin | acute kidney injury | Mincle | TLR4/NF-κB/Syk signaling | Clec4e | FIBROSIS | TLR4/NF-kappa B/Syk signaling | ACTIVATION | DENDRITIC CELLS | DEPLETION | NLRP3 INFLAMMASOME | DIPHTHERIA-TOXIN | ROLES | KIDNEY INJURY | UROLOGY & NEPHROLOGY | ABLATION | INNATE IMMUNITY | Ureteral Obstruction - complications | Kidney - pathology | Receptors, Pattern Recognition - immunology | Humans | Antigens, CD - metabolism | Lectins, C-Type - metabolism | Kidney - metabolism | RNA Interference | Time Factors | Acute Kidney Injury - immunology | Binding Sites | Disease Models, Animal | Macrophages - pathology | Signal Transduction | Acute Kidney Injury - pathology | Membrane Proteins - genetics | Mice, Transgenic | Toll-Like Receptor 4 - metabolism | Macrophage Activation | Macrophages - metabolism | Phenotype | Receptors, Pattern Recognition - genetics | RAW 264.7 Cells | Mice | Acute Kidney Injury - metabolism | Nitric Oxide Synthase Type II - metabolism | Macrophages - transplantation | Nephritis - genetics | Kidney - immunology | Lectins, C-Type - immunology | Acute Kidney Injury - genetics | Nephritis - pathology | Adoptive Transfer | Lectins, C-Type - genetics | Receptors, Pattern Recognition - metabolism | Transfection | Nephritis - immunology | Membrane Proteins - metabolism | Macrophages - immunology | Promoter Regions, Genetic | Mice, Inbred C57BL | Gene Expression Regulation | Membrane Proteins - immunology | Cisplatin | Syk Kinase - metabolism | Animals | Transcription Factor RelA - metabolism | Antigens, Differentiation, Myelomonocytic - metabolism | Nephritis - metabolism
Journal Article
European Journal of Clinical Investigation, ISSN 0014-2972, 03/2016, Volume 46, Issue 3, pp. 213 - 226
Background MicroRNAs (miRNAs) contribute to chronic kidney disease (CKD) progression via regulating mRNAs involved in renal homeostasis. However, their... 
systems biology | transcriptomics | miRNA | Biomarker | chronic kidney disease | microarray | Chronic kidney disease | Microarray | Systems biology | Transcriptomics | MiRNA | MEDICINE, RESEARCH & EXPERIMENTAL | INJURY | RECEPTOR | ALPHA | DIABETIC-NEPHROPATHY | TNF | NERVE GROWTH-FACTOR | MEDICINE, GENERAL & INTERNAL | DEATH LIGAND TRAIL | INFLAMMATION | GENE-EXPRESSION | ISCHEMIA/REPERFUSION | Up-Regulation | Glomerulosclerosis, Focal Segmental - genetics | Humans | Middle Aged | Transcriptome | Glomerulonephritis, Membranous - genetics | Glomerulonephritis, IGA - genetics | Male | MicroRNAs - metabolism | Gene Expression Profiling | RNA, Messenger - metabolism | Glomerulonephritis, Membranous - metabolism | Renal Insufficiency, Chronic - metabolism | Young Adult | Kidney - metabolism | Renal Insufficiency, Chronic - genetics | Adult | Female | Lupus Nephritis - metabolism | Nephrosclerosis - genetics | Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis - metabolism | Glomerulonephritis, Membranoproliferative - metabolism | Real-Time Polymerase Chain Reaction | Nephrosis, Lipoid - metabolism | Lupus Nephritis - genetics | Nephrosclerosis - metabolism | Diabetic Nephropathies - metabolism | Down-Regulation | Diabetic Nephropathies - genetics | Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis - genetics | Nephrosis, Lipoid - genetics | Reverse Transcriptase Polymerase Chain Reaction | Glomerulosclerosis, Focal Segmental - metabolism | Glomerulonephritis, Membranoproliferative - genetics | Glomerulonephritis, IGA - metabolism | Aged | Cohort Studies
Journal Article
American Journal of Physiology - Renal Physiology, ISSN 0363-6127, 05/2014, Volume 306, Issue 9, pp. F970 - F980
Microvascular rarefaction, or loss of microvascular density, is increasingly implicated in the progression from acute ischemic kidney injury to chronic kidney... 
Chronic kidney disease | Mitochondrial cristae | SS-31 | Acute kidney injury | Szeto-schiller peptides | RESPIRATORY-CHAIN | chronic kidney disease | REVASCULARIZATION | PHYSIOLOGY | TUBULOINTERSTITIAL INJURY | REPERFUSION INJURY | Szeto-Schiller peptides | PROLIFERATION | MODEL | mitochondrial cristae | PERITUBULAR CAPILLARIES | CHRONIC HYPOXIA | UROLOGY & NEPHROLOGY | acute kidney injury | RABBIT HEART | Kidney - blood supply | Mitochondrial Swelling - drug effects | Microvessels - metabolism | Reperfusion Injury - drug therapy | Male | Nephritis - prevention & control | Nephritis - pathology | Mitochondria - ultrastructure | Recovery of Function | Mitochondrial Membranes - drug effects | Renal Insufficiency, Chronic - metabolism | Endothelial Cells - ultrastructure | Kidney - metabolism | Time Factors | Adenosine Triphosphate - metabolism | Reperfusion Injury - metabolism | Kidney - physiopathology | Cytoprotection | Disease Models, Animal | Microvessels - ultrastructure | Kidney - drug effects | Nephritis - physiopathology | Reperfusion Injury - pathology | Acute Kidney Injury - pathology | Endothelial Cells - metabolism | Microvessels - drug effects | Rats | Cardiolipins - metabolism | Mitochondria - metabolism | Mitochondria - drug effects | Oligopeptides - metabolism | Acute Kidney Injury - physiopathology | Rats, Sprague-Dawley | Acute Kidney Injury - prevention & control | Disease Progression | Kidney - ultrastructure | Mitochondrial Membranes - metabolism | Renal Insufficiency, Chronic - pathology | Renal Insufficiency, Chronic - prevention & control | Animals | Fibrosis | Mitochondrial Membranes - ultrastructure | Reperfusion Injury - physiopathology | Nephritis - metabolism | Acute Kidney Injury - metabolism | Oligopeptides - pharmacology | Energy Metabolism - drug effects | Endothelial Cells - drug effects | Physiological aspects | Inflammation | Kidney diseases | Ischemia
Journal Article