ReviewCell communication and signaling : CCS2024
Crosstalk among podocytes, glomerular endothelial cells and mesangial cells in diabetic kidney disease: an updated review.
Review in Cell communication and signaling : CCS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers, 4 of them syntheses that pooled it.
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The trial behind it
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Who cites it
90 citing papers in PubMed, 4 syntheses or guidelines pooled it, 95 citations in OpenAlex.
- Exosomes in diabetic kidney disease: pathogenesis, biomarker discovery, and emerging therapeutics-a comprehensive systematic review.Renal failure · 2026Pooled it
- Focus on podocytes: diabetic kidney disease and renal fibrosis - a global bibliometric analysis (2000-2024).Frontiers in pharmacology · 2024Pooled it
- The efficacy and safety ofFrontiers in pharmacology · 2024Pooled it
- Lipid homeostasis in diabetic kidney disease.International journal of biological sciences · 2024Pooled it
- Integrative multi-omics analysis identifies VCAN and ESM1 as candidate cell-type-associated biomarkers of NET-related glomerular injury in diabetic kidney disease.Renal failure · 2026Article
- Combined podocyte, fibrotic and echocardiographic correlates of an operationally defined subclinical cardiorenal phenotype in chronic kidney disease: an exploratory study.Renal failure · 2026Observational
- Silencing of USP22 promotes FGF11 degradation to attenuates renal fibrosis in diabetic kidney disease.Renal failure · 2026Article
- The dual role of exosomes in renal fibrosis and their potential for clinical translational applications.Renal failure · 2026Review
- M1 macrophage-derived exosomes aggravate diabetic nephropathy by regulating the WTAP/S1PR2 axis.Journal of diabetes investigation · 2026Article
- Perirenal fat β₃-adrenergic signaling alleviates renal fibrosis via regulating Bcat2/BCAA-TNFα pathway in diabetic kidney disease.Nature communications · 2026Article
- Baicalein alleviates high glucose-induced mesangial cell fibrosis and inflammation in diabetic nephropathy: roles of AMPK activation and TGF-β1 inhibition.Genes & genomics · 2026Article
- Urinary Extracellular Vesicle-Derived miRNAs as Regulators and Biomarkers in Diabetic Kidney Disease.International journal of molecular sciences · 2026Review
- Reappraising Kidney Biopsy in Diabetic Kidney Disease: Histopathology, Clinical Course, and the Future of Precision Nephrology.Journal of clinical medicine · 2026Review
- Article
- Glomerulo-Tubular Crosstalk in Diabetic Kidney Disease: From Pathophysiology to Novel Therapeutics.Electrolyte & blood pressure : E & BP · 2026Review
- Molecular mechanisms and therapeutic strategies of glomerular cell senescence in diabetic kidney disease: from heterogeneity to precision intervention.Cellular and molecular life sciences : CMLS · 2026Review
- Beyond the Cell Atlas: Functional Communities as the Essential Pathologic Units Driving Kidney Disease.Journal of the American Society of Nephrology : JASN · 2026Review
- RAB27A silencing modulates miR-30d-5p expression and extracellular vesicle non-coding RNA cargo in diabetic podocytes.Scientific reports · 2026Article
- Podocyte TLR4 deletion alleviates diabetic kidney disease through prohibiting PKCδ/SHP-1-dependent ER stress and relieving podocyte damage and inflammation.Journal of advanced research · 2026Article
- Association of endothelial activation and stress index with all-cause and cardiovascular mortality in patients with diabetic kidney disease: a population-based prospective study.Diabetology & metabolic syndrome · 2026Article
30 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
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetic kidney disease (DKD) is a long-term and serious complication of diabetes that affects millions of people worldwide. It is characterized by proteinuria, glomerular damage, and renal fibrosis, leading to end-stage renal disease, and the pathogenesis is complex and involves multiple cellular and molecular mechanisms. Among three kinds of intraglomerular cells including podocytes, glomerular endothelial cells (GECs) and mesangial cells (MCs), the alterations in one cell type can produce changes in the others. The cell-to-cell crosstalk plays a crucial role in maintaining the glomerular filtration barrier (GFB) and homeostasis. In this review, we summarized the recent advances in understanding the pathological changes and interactions of these three types of cells in DKD and then focused on the signaling pathways and factors that mediate the crosstalk, such as angiopoietins, vascular endothelial growth factors, transforming growth factor-β, Krüppel-like factors, retinoic acid receptor response protein 1 and exosomes, etc. Furthermore, we also simply introduce the application of the latest technologies in studying cell interactions within glomerular cells and new promising mediators for cell crosstalk in DKD. In conclusion, this review provides a comprehensive and updated overview of the glomerular crosstalk in DKD and highlights its importance for the development of novel intervention approaches.
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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.