ReviewCell and tissue research2012
Mechanisms and consequences of TGF-ß overexpression by podocytes in progressive podocyte disease.
Review in Cell and tissue research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
39 citing papers in PubMed, 96 citations in OpenAlex.
- Fresolimumab treatment decreases biomarkers and improves clinical symptoms in systemic sclerosis patients.The Journal of clinical investigation · 2015Trial
- Single-Nucleus Transcriptomic Atlas Reveals Disease-Associated Cellular States in Human Glomerular Diseases.Kidney international reports · 2026Article
- A new brake on podocyte injury: ATOH8 meets TGF-β.American journal of physiology. Renal physiology · 2026Article
- Upregulation of angiotensin-(1-7) formation in human podocytes - enzyme activity assay upon fluid flow shear stress.PloS one · 2026Article
- Oxidative Stress and Nutritional Antioxidants in Renal Diseases: A Narrative Review.Antioxidants (Basel, Switzerland) · 2025Review
- Systemic inflammation accelerates the development of focal segmental glomerulosclerosis in a mouse model of adriamycin induced nephrosis.Scientific reports · 2025Article
- Finerenone Ameliorates High Glucose-Induced Podocytes Epithelial-Mesenchymal Transition Through the Regulation of Krüppel-Like Factor 5 in Diabetic Nephropathy.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025Article
- Urolithin A Ameliorates the TGF Beta-Dependent Impairment of Podocytes Exposed to High Glucose.Journal of personalized medicine · 2024Article
- Hidden genetics behind glomerular scars: an opportunity to understand the heterogeneity of focal segmental glomerulosclerosis?Pediatric nephrology (Berlin, Germany) · 2024Review
- Ghrelin hormone a new molecular modulator between obesity and glomerular damage.Molecular biology reports · 2023Review
- Btg2 Promotes Focal Segmental Glomerulosclerosis via Smad3-Dependent Podocyte-Mesenchymal Transition.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- The role of the immune system in idiopathic nephrotic syndrome.Molecular and cellular pediatrics · 2021Review
- Development of Biomarkers and Molecular Therapy Based on Inflammatory Genes in Diabetic Nephropathy.International journal of molecular sciences · 2021Review
- Gestational and Breastfeeding Low-Protein Intake on Blood Pressure, Kidney Structure, and Renal Function in Male Rat Offspring in Adulthood.Frontiers in physiology · 2021Article
- Therapeutic Insights in Chronic Kidney Disease Progression.Frontiers in medicine · 2021Review
- ECM Characterization Reveals a Massive Activation of Acute Phase Response during FSGS.International journal of molecular sciences · 2020Article
- Evaluation of Serum microRNAs in Patients with Diabetic Kidney Disease: A Nested Case-Controlled Study and Bioinformatics Analysis.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- Mitotic Catastrophe Causes Podocyte Loss in the Urine of Human Diabetics.The American journal of pathology · 2019Article
- Markers of renal fibrosis: How do they correlate with podocyte damage in glomerular diseases?PloS one · 2019Article
- Brain natriuretic peptide mitigates TIMP2 induction and reinstates extracellular matrix catabolic activityAmerican journal of translational research · 2019Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In patients with progressive podocyte disease, such as focal segmental glomerulosclerosis (FSGS) and membranous nephropathy, upregulation of transforming growth factor-ß (TGF-ß) is observed in podocytes. Mechanical pressure or biomechanical strain in podocytopathies may cause overexpression of TGF-ß and angiotensin II (Ang II). Oxidative stress induced by Ang II may activate the latent TGF-ß, which then activates Smads and Ras/extracellular signal-regulated kinase (ERK) signaling pathways in podocytes. Enhanced TGF-ß activity in podocytes may lead to thickening of the glomerular basement membrane (GBM) by overproduction of GBM proteins and impaired GBM degradation in podocyte disease. It may also lead to podocyte apoptosis and detachment from the GBM, and epithelial-mesenchymal transition (EMT) of podocytes, initiating the development of glomerulosclerosis. Furthermore, activated TGF-ß/Smad signaling by podocytes may induce connective tissue growth factor and vascular endothelial growth factor overexpression, which could act as a paracrine effector mechanism on mesangial cells to stimulate mesangial matrix synthesis. In proliferative podocytopathies, such as cellular or collapsing FSGS, TGF-ß-induced ERK activation may play a role in podocyte proliferation, possibly via TGF-ß-induced EMT of podocytes. Collectively, these data bring new mechanistic insights into our understanding of the TGF-ß overexpression by podocytes in progressive podocyte disease.
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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 Socratic graph.