ReviewCurrent opinion in nephrology and hypertension2010
Intratubular hydrodynamic forces influence tubulointerstitial fibrosis in the kidney.
Review in Current opinion in nephrology and hypertension, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
31 citing papers in PubMed, 55 citations in OpenAlex.
- Research progress on the mechanism of renal interstitial fibrosis in obstructive nephropathy.Heliyon · 2023Review
- Editorial: Insights in renal and epithelial physiology: 2021.Frontiers in physiology · 2022Article
- A 3D Renal Proximal Tubule on Chip Model Phenocopies Lowe Syndrome and Dent II Disease Tubulopathy.International journal of molecular sciences · 2021Article
- The Genomic Response to TGF-β1 Dictates Failed Repair and Progression of Fibrotic Disease in the Obstructed Kidney.Frontiers in cell and developmental biology · 2021Review
- The serum amyloid A3 promoter-driven luciferase reporter mice is a valuable tool to image early renal fibrosis development and shows the therapeutic effect of glucosyl-hesperidin treatment.Scientific reports · 2019Article
- Profibrotic epithelial phenotype: a central role for MRTF and TAZ.Scientific reports · 2019Article
- Glycemic control by the SGLT2 inhibitor empagliflozin decreases aortic stiffness, renal resistivity index and kidney injury.Cardiovascular diabetology · 2018Article
- Deregulation of Hippo-TAZ pathway during renal injury confers a fibrotic maladaptive phenotype.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
- Comprehensive transcriptome analysis of fluid shear stress altered gene expression in renal epithelial cells.Journal of cellular physiology · 2018Article
- TGF-β1/p53 signaling in renal fibrogenesis.Cellular signalling · 2018Review
- Cdc42 activation couples fluid shear stress to apical endocytosis in proximal tubule cells.Physiological reports · 2017Article
- Fluid shear stress-induced TGF-β/ALK5 signaling in renal epithelial cells is modulated by MEK1/2.Cellular and molecular life sciences : CMLS · 2017Article
- Lung Microtissue Array to Screen the Fibrogenic Potential of Carbon Nanotubes.Scientific reports · 2016Article
- Urinary active transforming growth factor β in feline chronic kidney disease.Veterinary journal (London, England : 1997) · 2016Article
- Article
- Obesity Correlates With Glomerulomegaly But Is Not Associated With Kidney Dysfunction Early After Donation.Transplantation direct · 2015Article
- Shear Stress-Induced Alteration of Epithelial Organization in Human Renal Tubular Cells.PloS one · 2015Article
- Emerging urinary markers of renal injury in obstructive nephropathy.BioMed research international · 2014Review
- Piezo1-dependent stretch-activated channels are inhibited by Polycystin-2 in renal tubular epithelial cells.EMBO reports · 2013Article
- Tissue mechanics and fibrosis.Biochimica et biophysica acta · 2013Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
purpose of reviewRenal epithelial cells respond to mechanical stimuli with immediate transduction events (e.g. activation of ion channels), intermediate biological responses (e.g. changes in gene expression), and long-term cellular adaptation (e.g. protein expression). Progressive renal disease is characterized by disturbed glomerular hydrodynamics that contributes to glomerulosclerosis, but how intratubular biomechanical forces contribute to tubulointerstital inflammation and fibrosis is poorly understood. RECENT
findingsIn-vivo and in-vitro models of obstructive uropathy demonstrate that tubular stretch induces robust expression of transforming growth factor beta-1, activation of tubular apoptosis, and induction of nuclear factor-kappaB signaling, which contribute to the inflammatory and fibrotic milieu. Nonobstructive structural kidney diseases associated with nephron loss follow a course characterized by compensatory increases of single nephron glomerular filtration rate and tubular flow rate. Resulting increases in tubular fluid shear stress reduce tissue-plasminogen activator and urokinase enzymatic activity, which diminishes breakdown of extracellular matrix. In models of high dietary Na intake, which increases tubular flow, urinary transforming growth factor beta-1 concentrations and renal mitogen-activated protein kinase activity are increased. SUMMARY: In conclusion, intratubular biomechanical forces, stretch, and fluid shear stress generate changes in intracellular signaling and gene expression that contribute to the pathobiology of obstructive and nonobstructive kidney disease.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.