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International Journal of Biological Sciences, ISSN 1449-2288, 2011, Volume 7, Issue 7, pp. 1056 - 1067
Journal Article
Circulation, ISSN 0009-7322, 01/2019, Volume 139, Issue 5, pp. 718 - 719
Journal Article
Journal Article
Clinical and Experimental Pharmacology & Physiology, ISSN 0305-1870, 08/2012, Volume 39, Issue 8, p. 731
  Summary Diabetic nephropathy (DN) is a major diabetic complication that is mediated by transforming growth factor (TGF)-[beta]1 via Smad-dependent and... 
Journal Article
Clinical and Experimental Pharmacology and Physiology, ISSN 0305-1870, 08/2012, Volume 39, Issue 8, p. 731
Diabetic nephropathy (DN) is a major diabetic complication that is mediated by transforming growth factor (TGF)-[beta]1 via Smad-dependent and -independent... 
MicroRNA | Diabetic nephropathies | Angiotensin | Mitogens | Growth factors
Journal Article
Advances in experimental medicine and biology, ISSN 0065-2598, 2019, Volume 1165, p. 285
Monocytes/macrophages are highly involved in the process of renal injury, repair and fibrosis in many aspects of experimental and human renal diseases.... 
Kidney Diseases - physiopathology | Myofibroblasts - cytology | Monocytes | Kidney - pathology | Humans | Fibrosis | Cell Differentiation | Macrophages - cytology
Journal Article
Sheng li xue bao : [Acta physiologica Sinica], ISSN 0371-0874, 12/2018, Volume 70, Issue 6, p. 612
Transforming growth factor-β (TGF-β) is a driving force of renal fibrosis, which may lead to chronic kidney diseases and even end stage renal diseases. By... 
Signal Transduction | Kidney Diseases - pathology | Epigenesis, Genetic | Humans | Fibrosis | Smad3 Protein - metabolism | Transforming Growth Factor beta - metabolism | Smad7 Protein - metabolism
Journal Article
Sheng li xue bao : [Acta physiologica Sinica], ISSN 0371-0874, 12/2018, Volume 70, Issue 6, pp. 612 - 622
Journal Article
by Meng, XM and Tang, PMK and Li, J and Lan, HY
FRONTIERS IN PHYSIOLOGY, ISSN 1664-042X, 03/2015, Volume 6, p. 82
TGF-beta (transforming growth factor-beta) is well identified as a central mediator in renal fibrosis. TGF-beta initiates canonical and non-canonical pathways... 
CRESCENTIC GLOMERULONEPHRITIS | therapeutics | PHYSIOLOGY | DIABETIC-NEPHROPATHY | renal fibrosis | MESENCHYMAL TRANSITION | TGF-beta | GROWTH-FACTOR-BETA | TRANSFORMING GROWTH-FACTOR-BETA-1 | MOUSE MODEL | THERAPEUTIC TARGET | LATENT TGF-BETA-1 | GENE-TRANSFER | Smads mediators | CHRONIC KIDNEY-DISEASE | mechanisms | TGF-β | Smads Mediators | Therapeutics
Journal Article
Small, ISSN 1613-6810, 10/2019, p. 1903674
Journal Article
PLoS ONE, ISSN 1932-6203, 07/2013, Volume 8, Issue 7, p. e70195
Journal Article
Kidney International, ISSN 0085-2538, 03/2018, Volume 93, Issue 3, pp. 568 - 579
Renal tubules are the major component of the kidney and are vulnerable to a variety of injuries including hypoxia, proteinuria, toxins, metabolic disorders,... 
chronic kidney disease | acute kidney injury | renal fibrosis | renal tubule | renal inflammation | ACTIVATED PROTEIN-KINASE | CELL-CYCLE ARREST | GLOMERULAR EPITHELIAL-CELLS | ISCHEMIA-REPERFUSION INJURY | TO-MESENCHYMAL TRANSITION | TISSUE GROWTH-FACTOR | RENIN-ANGIOTENSIN SYSTEM | II-INDUCED HYPERTROPHY | UROLOGY & NEPHROLOGY | NF-KAPPA-B | PERICYTE-MYOFIBROBLAST TRANSITION | Cell Proliferation | Epithelial Cells - metabolism | Renal Insufficiency, Chronic - etiology | Humans | Renal Insufficiency, Chronic - metabolism | Acute Kidney Injury - complications | Epithelial-Mesenchymal Transition | Inflammation Mediators - metabolism | Acute Kidney Injury - immunology | Kidney Tubules - pathology | Kidney Tubules - metabolism | Cytokines - immunology | Inflammation Mediators - immunology | Kidney Tubules - immunology | Renal Insufficiency, Chronic - immunology | Cytokines - metabolism | Signal Transduction | Acute Kidney Injury - pathology | Cell Cycle Proteins - metabolism | Epithelial Cells - pathology | Immunity, Innate | Disease Progression | Renal Insufficiency, Chronic - pathology | Cell Cycle Checkpoints | Animals | Energy Metabolism | Epithelial Cells - immunology | Fibrosis | Acute Kidney Injury - metabolism | Senescence | Kidneys | Immune response | Mesenchyme | Epithelial cells | Inflammation | Epithelium | Drug development | Renal tubules | Cell death | Hypoxia | Metabolic disorders | Proteinuria
Journal Article