ReviewRenal failure2017
Molecular mechanisms involved in podocyte EMT and concomitant diabetic kidney diseases: an update.
Review in Renal failure, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.
What it found
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Who cites it
72 citing papers in PubMed, 142 citations in OpenAlex.
- Single-cell and high-resolution spatial profiling of podocytopathies reveals core mechanisms of podocyte injury.Science advances · 2026Article
- Urinary ANGPTL3: a novel noninvasive biomarker for podocyte injury in pediatric glomerular diseases.Journal of translational medicine · 2026Article
- PLCε regulates podocyte differentiation and TGF-β1 responses via alteration of SMAD2/SMAD3 ratio.Cell communication and signaling : CCS · 2026Article
- Extracellular Vesicles Facilitate the Crosstalk Between High Glucose-Stimulated Mesangial Cells and Healthy Podocytes to Mediate Injury Responses.International journal of molecular sciences · 2026Article
- Renal Single-Cell RNA Sequencing and Digital Cytometry in Dogs with X-Linked Hereditary Nephropathy.Animals : an open access journal from MDPI · 2025Article
- Progress in the application of mesenchymal stem cells to attenuate apoptosis in diabetic kidney disease.World journal of diabetes · 2025Review
- Therapeutic role of miR-26a on cardiorenal injury in a mice model of angiotensin-II induced chronic kidney disease through inhibition of LIMS1/ILK pathway.Chinese medical journal · 2025Article
- FSTL1 aggravates high glucose-induced oxidative stress and transdifferentiation in HK-2 cells.Scientific reports · 2025Article
- Targeting Fibrosis: From Molecular Mechanisms to Advanced Therapies.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Transcriptomics and Proteomics Reveal That TLPW Acupuncture Ameliorates Proteinuria in Diabetic Kidney Disease Model Rats by Suppressing Epithelial-to-Mesenchymal Transition via the DPP4/SDF-1Journal of diabetes research · 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
- Shionone Inhibits Glomerular Fibirosis by Suppressing NLRP3 Related Inflammasome though SESN2-NRF2/ HO-1 Pathway.Diabetes & metabolism journal · 2025Article
- Notch signaling in diabetic kidney disease: recent progress.Frontiers in endocrinology · 2025Review
- Histone methylation modification and diabetic kidney disease: Potential molecular mechanisms and therapeutic approaches (Review).International journal of molecular medicine · 2024Review
- Urolithin A Ameliorates the TGF Beta-Dependent Impairment of Podocytes Exposed to High Glucose.Journal of personalized medicine · 2024Article
- Role of Extracellular Vesicle-Derived Noncoding RNAs in Diabetic Kidney Disease.Kidney diseases (Basel, Switzerland) · 2024Review
- Obesity-related glomerulopathy is associated with elevated WT1 expression in podocytes.International journal of obesity (2005) · 2024Article
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- Exosomes derived from mesenchymal stem cells in diabetes and diabetic complications.Cell death & disease · 2024Review
12 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epithelial-mesenchymal transition (EMT) is a tightly regulated process by which epithelial cells lose their hallmark epithelial characteristics and gain the features of mesenchymal cells. For podocytes, expression of nephrin, podocin, P-cadherin, and ZO-1 is downregulated, the slit diaphragm (SD) will be altered, and the actin cytoskeleton will be rearranged. Diabetes, especially hyperglycemia, has been demonstrated to incite podocyte EMT through several molecular mechanisms such as TGF-β/Smad classic pathway, Wnt/β-catenin signaling pathway, Integrins/integrin-linked kinase (ILK) signaling pathway, MAPKs signaling pathway, Jagged/Notch signaling pathway, and NF-κB signaling pathway. As one of the most fundamental prerequisites to develop ground-breaking therapeutic options to prevent the development and progression of diabetic kidney disease (DKD), a comprehensive understanding of the molecular mechanisms involved in the pathogenesis of podocyte EMT is compulsory. Therefore, the purpose of this paper is to update the research progress of these underlying signaling pathways and expound the podocyte EMT-related DKDs.
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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 Socratic graph.