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Kidney International, ISSN 0085-2538, 08/2012, Volume 82, Issue 4, pp. 412 - 427
Endothelial progenitor cells are known to reverse acute kidney injury by paracrine mechanisms. We previously found that microvesicles released from these... 
exosome | ischemia–reperfusion | acute kidney injury | ischemia-reperfusion | HORIZONTAL TRANSFER | STEM-CELLS | CONTRIBUTE | REGENERATION | FAILURE | EXPERIMENTAL GLOMERULONEPHRITIS | REPAIR | EPITHELIAL-CELLS | MESSENGER-RNA | UROLOGY & NEPHROLOGY | PLATELET-ACTIVATING-FACTOR | Chemotaxis, Leukocyte | Cell Proliferation | Epithelial Cells - metabolism | Kidney - blood supply | Capillaries - pathology | Kidney - pathology | Rats, Wistar | Endothelial Cells - transplantation | Cell-Derived Microparticles - transplantation | Male | MicroRNAs - metabolism | Acute Kidney Injury - genetics | Stem Cells - metabolism | Cell Hypoxia | Stem Cell Transplantation | Kidney - metabolism | Transfection | RNA Interference | Time Factors | Cell-Derived Microparticles - pathology | Cell-Derived Microparticles - metabolism | Kidney Tubules - pathology | Kidney Tubules - metabolism | Capillaries - metabolism | Reperfusion Injury - genetics | Reperfusion Injury - metabolism | Disease Models, Animal | Ribonuclease III - genetics | Ribonuclease III - metabolism | Reperfusion Injury - pathology | Acute Kidney Injury - pathology | Endothelial Cells - metabolism | Cells, Cultured | Gene Expression Regulation | Rats | Epithelial Cells - pathology | Acute Kidney Injury - prevention & control | Regeneration | Oligonucleotides - metabolism | Animals | Reperfusion Injury - prevention & control | Fibrosis | Stem Cells - pathology | Acute Kidney Injury - metabolism | Endothelial Cells - pathology | Apoptosis | Index Medicus | Cell proliferation | Intravenous administration | Paracrine signalling | mRNA | Leukocytes | Ribonuclease | Endothelial cells | Kidney | Angiogenesis | Ischemia | Stem cells | Hypoxia | miRNA | Capillaries | Injuries
Journal Article
Journal of the American Society of Nephrology, ISSN 1046-6673, 2009, Volume 20, Issue 12, pp. 2593 - 2603
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 | Index Medicus
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 | Index Medicus
Journal Article
European Journal of Clinical Investigation, ISSN 0014-2972, 03/2016, Volume 46, Issue 3, pp. 213 - 226
BackgroundMicroRNAs (miRNAs) contribute to chronic kidney disease (CKD) progression via regulating mRNAs involved in renal homeostasis. However, their... 
systems biology | transcriptomics | Biomarker | chronic kidney disease | microarray | RNA | 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 | miRNA | 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 | Index Medicus
Journal Article
Journal Article
Biochemical and Biophysical Research Communications, ISSN 0006-291X, 04/2017, Volume 486, Issue 2, pp. 499 - 505
Short-chain fatty acids (SCFAs), such as acetate, propionate, and butyrate, are produced predominantly by gut microbiota fermentation of dietary fiber. SCFAs... 
GPR41 | Monocyte chemoattractant protein-1 | p38 | SCFA | GPR43 | JNK | CYTOKINES | BIOCHEMISTRY & MOLECULAR BIOLOGY | GUT MICROBIOTA | PROPIONATE | HISTONE DEACETYLATION | BIOPHYSICS | METABOLISM | SODIUM-BUTYRATE | ACCUMULATION | MEDIATORS | ACETATE | NF-KAPPA-B | Fatty Acids, Volatile - pharmacology | Tumor Necrosis Factor-alpha - metabolism | Kidney Cortex - drug effects | RNA, Small Interfering - genetics | Epithelial Cells - metabolism | Receptors, G-Protein-Coupled - metabolism | Kidney Cortex - metabolism | Epithelial Cells - drug effects | Humans | Tumor Necrosis Factor-alpha - genetics | Glomerulonephritis - metabolism | Fatty Acids, Volatile - metabolism | MAP Kinase Kinase 4 - metabolism | Chemokine CCL2 - metabolism | p38 Mitogen-Activated Protein Kinases - metabolism | Phosphorylation - drug effects | Cell Line | Signal Transduction | Gene Expression Regulation | Glomerulonephritis - genetics | Kidney Tubules, Collecting - pathology | Receptors, Cell Surface - metabolism | p38 Mitogen-Activated Protein Kinases - genetics | Chemokine CCL2 - genetics | Epithelial Cells - pathology | Kidney Cortex - pathology | Kidney Tubules, Collecting - metabolism | Glomerulonephritis - pathology | MAP Kinase Kinase 4 - genetics | Receptors, G-Protein-Coupled - genetics | RNA, Small Interfering - metabolism | Receptors, Cell Surface - genetics | Index Medicus
Journal Article
Scientific Reports, ISSN 2045-2322, 02/2017, Volume 7, Issue 1, pp. 43409 - 43409
The role of p53 in renal fibrosis has recently been suggested, however, its function remains controversial and the underlying mechanism is unclear. Here, we... 
ACUTE KIDNEY INJURY | TARGET GENES | TGF-BETA | INHIBITION | CANCER CELLS | OBSTRUCTIVE NEPHROPATHY | MULTIDISCIPLINARY SCIENCES | INTERSTITIAL FIBROBLAST ACTIVATION | CELL-CYCLE ARREST | NUCLEAR TRANSLOCATION | SIGNAL TRANSDUCER | Epithelial Cells - metabolism | Kidney - pathology | Vimentin - metabolism | Epithelial Cells - drug effects | Humans | Transforming Growth Factor beta1 - metabolism | Urethral Obstruction - genetics | Glomerulonephritis, IGA - genetics | Male | MicroRNAs - metabolism | Tumor Suppressor Protein p53 - genetics | Kidney - metabolism | Urethra - pathology | Collagen Type I - genetics | Vimentin - genetics | Urethral Obstruction - metabolism | Nuclear Proteins - genetics | Glomerulonephritis, IGA - pathology | STAT3 Transcription Factor - genetics | STAT3 Transcription Factor - metabolism | Disease Models, Animal | Cell Line | Diabetic Nephropathies - pathology | Collagen Type I - metabolism | Signal Transduction | Diabetic Nephropathies - metabolism | Mice, Inbred C57BL | Gene Expression Regulation | Tumor Suppressor Protein p53 - metabolism | Suppressor of Cytokine Signaling Proteins - genetics | Diabetic Nephropathies - genetics | Epithelial Cells - pathology | Nuclear Proteins - metabolism | Transforming Growth Factor beta1 - genetics | Animals | Urethral Obstruction - pathology | Fibrosis | Glomerulonephritis, IGA - metabolism | Urethra - metabolism | Mice | MicroRNAs - genetics | Suppressor of Cytokine Signaling Proteins - metabolism | Vimentin | Phosphorylation | Collagen (type I) | Epithelial cells | p53 Protein | Diabetes mellitus | Stat3 protein | Chromosome 3 | Immunoglobulin A | IgA nephropathy | Overexpression | Collagen | Rodents | Apoptosis | Kidney transplantation | Index Medicus
Journal Article
Nephrology Dialysis Transplantation, ISSN 0931-0509, 08/2012, Volume 27, Issue 8, pp. 3234 - 3241
Journal Article
Science, ISSN 0036-8075, 6/2005, Volume 308, Issue 5729, pp. 1801 - 1804
Focal and segmental glomerulosclerosis (FSGS) is a kidney disorder of unknown etiology, and up to 20% of patients on dialysis have been diagnosed with it. Here... 
Receptors | Kidneys | Messenger RNA | Focal segmental glomerulosclerosis | Calcium | HEK293 cells | Cell lines | Reports | Kidney cells | Kidney diseases | Genetic mutation | INSERTION | PROTEIN | SLIT DIAPHRAGM | NEPHRIN | MULTIDISCIPLINARY SCIENCES | GENETIC-HETEROGENEITY | PODOCIN | NEPHROTIC SYNDROME | EXPRESSION | ALPHA-ACTININ-4 | GLOMERULAR-DISEASE | Haplotypes | Uridine Triphosphate - metabolism | Calcium Channels - metabolism | Calcium - metabolism | Exons | Glomerulosclerosis, Focal Segmental - genetics | Humans | Male | Mutation, Missense | Sodium - metabolism | Kidney - metabolism | Receptor, Angiotensin, Type 1 - genetics | Transfection | Kidney Glomerulus - metabolism | Female | Cell Membrane - metabolism | GTP-Binding Protein alpha Subunits, Gq-G11 - metabolism | Kidney Tubules - metabolism | Calcium Channels - genetics | Calcium Signaling | Cell Line | Angiotensin II - pharmacology | TRPC6 Cation Channel | Angiotensin II - metabolism | TRPC Cation Channels | Uridine Triphosphate - pharmacology | Chromosomes, Human, Pair 11 - genetics | Sequence Analysis, DNA | Carbachol - pharmacology | Patch-Clamp Techniques | Pedigree | Calcium Channels - chemistry | Receptor, Angiotensin, Type 1 - metabolism | Amino Acid Substitution | Glomerulonephritis | Case studies | Research | Analysis | Heredity | Mutation | Chromosomes | Genes | Index Medicus
Journal Article
Kidney International, ISSN 0085-2538, 11/2014, Volume 86, Issue 5, pp. 965 - 978
Interleukin (IL)-1β contributes to renal injury in immune complex glomerulonephritis. However, production of mature IL-1β depends on activation of the... 
cytokines | interleukin 1 | dendritic cell | nephrotoxic serum nephritis | KIDNEY-DISEASE | RECRUITMENT | ACTIVATION | MURINE CRESCENTIC GLOMERULONEPHRITIS | DENDRITIC CELLS | GLOMERULAR INJURY | TUMOR-NECROSIS-FACTOR | RENAL INFLAMMATION | UROLOGY & NEPHROLOGY |