ArticleJCI insight2020
Role of ultrastructural determinants of glomerular permeability in ultrafiltration function loss.
Article in JCI insight, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 30 citations in OpenAlex.
- A scanning electron microscopy-based approach to explore subpodocyte space remodeling in diabetic kidneys of mice and humans.Scientific reports · 2026Article
- A Tissue Engineering's Guide to Biomimicry.Macromolecular bioscience · 2025Review
- The integrin repertoire drives YAP-dependent epithelial:stromal interactions during injury of the kidney glomerulus.Nature communications · 2025Article
- Albuminuria in Cardiovascular, Kidney, and Metabolic Disorders: A State-of-the-Art Review.Circulation · 2025Review
- Integrins in the kidney - beyond the matrix.Nature reviews. Nephrology · 2025Review
- Numerical Flow Simulations of the Shear Stress Forces Arising in Filtration Slits during Glomerular Filtration in Rat Kidney.Journal of the American Society of Nephrology : JASN · 2025Article
- The Lipid-Oxidative Stress Axis: Novel Therapeutic Targets for Podocytopathy.Journal of inflammation research · 2025Review
- Glomerular hyperfiltration.Nature reviews. Nephrology · 2022Review
- Metabolic Syndrome and β-Oxidation of Long-Chain Fatty Acids in the Brain, Heart, and Kidney Mitochondria.International journal of molecular sciences · 2022Review
- Imaging the Kidney with an Unconventional Scanning Electron Microscopy Technique: Analysis of the Subpodocyte Space in Diabetic Mice.International journal of molecular sciences · 2022Article
- Unravelling the Role of PAX2 Mutation in Human Focal Segmental Glomerulosclerosis.Biomedicines · 2021Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The epithelial filtration slit is a crucial component of the glomerular capillary membrane, which is essential for maintaining glomerular filtration function. Though chronic kidney diseases are an immense clinical problem, the mechanisms through which structural alterations reduce glomerular water filtration have not yet been understood completely. To investigate the mechanisms underlying filtration function loss, we studied rats with spontaneously occurring progressive kidney disease, either treated with angiotensin II antagonist or untreated, combining high-resolution electron microscopy of the glomerular capillary wall with theoretical water filtration modeling. Under pathological conditions, epithelial filtration pores and the extension of the subpodocyte space were larger than in normal controls. Numerical analyses indicated that these ultrastructural changes increased hydraulic resistance of the glomerular capillary wall by extending coverage of the filtration barrier by the subpodocyte space, with the changes in hydrodynamic forces acting on podocytes likely being responsible for their detachment. Angiotensin II inhibition normalized the subpodocyte space's hydraulic resistance, restored mechanical podocyte load, and preserved CD151-α3 integrin complex assembly, improving podocyte adherence and survival. Our results show that ultrastructural changes in podocytes are major determinants of the hydraulic resistance of the glomerular capillary wall and highlight the mechanism of podocyte loss in kidney disease progression, as well as the mechanisms underlying angiotensin II inhibition.
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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.