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Relevant bibliographies by topics / Glomerular Filtration Barrier

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Academic literature on the topic 'Glomerular Filtration Barrier'

Author: Grafiati

Published: 4 June 2021

Last updated: 28 July 2025

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Journal articles on the topic "Glomerular Filtration Barrier"

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Haraldsson, Börje, and Marie Jeansson. "Glomerular filtration barrier." Current Opinion in Nephrology and Hypertension 18, no. 4 (2009): 331–35. http://dx.doi.org/10.1097/mnh.0b013e32832c9dba.

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Rani Verma, Reena. "Glomerular Filtration Barrier and Mechanism of Proteinuria." International Physiology 8, no. 1 (2020): 27–29. http://dx.doi.org/10.21088/ip.2347.1506.8120.4.

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‘t Hart, Daan C., Dilemin Yildiz, Valentina Palacio-Castañeda, et al. "Co-Culture of Glomerular Endothelial Cells and Podocytes in a Custom-Designed Glomerulus-on-a-Chip Model Improves the Filtration Barrier Integrity and Affects the Glomerular Cell Phenotype." Biosensors 13, no. 3 (2023): 339. http://dx.doi.org/10.3390/bios13030339.

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Crosstalk between glomerular endothelial cells and glomerular epithelial cells (podocytes) is increasingly becoming apparent as a crucial mechanism to maintain the integrity of the glomerular filtration barrier. However, in vitro studies directly investigating the effect of this crosstalk on the glomerular filtration barrier are scarce because of the lack of suitable experimental models. Therefore, we developed a custom-made glomerulus-on-a-chip model recapitulating the glomerular filtration barrier, in which we investigated the effects of co-culture of glomerular endothelial cells and podocyt

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Hausmann, Ralf, Martin Grepl, Volker Knecht, and Marcus J. Moeller. "The glomerular filtration barrier function." Current Opinion in Nephrology and Hypertension 21, no. 4 (2012): 441–49. http://dx.doi.org/10.1097/mnh.0b013e328354a28e.

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Scott, Rizaldy P., and Susan E. Quaggin. "The cell biology of renal filtration." Journal of Cell Biology 209, no. 2 (2015): 199–210. http://dx.doi.org/10.1083/jcb.201410017.

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The function of the kidney, filtering blood and concentrating metabolic waste into urine, takes place in an intricate and functionally elegant structure called the renal glomerulus. Normal glomerular function retains circulating cells and valuable macromolecular components of plasma in blood, resulting in urine with just trace amounts of proteins. Endothelial cells of glomerular capillaries, the podocytes wrapped around them, and the fused extracellular matrix these cells form altogether comprise the glomerular filtration barrier, a dynamic and highly selective filter that sieves on the basis

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Jarad, George, and Jeffrey H. Miner. "Update on the glomerular filtration barrier." Current Opinion in Nephrology and Hypertension 18, no. 3 (2009): 226–32. http://dx.doi.org/10.1097/mnh.0b013e3283296044.

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Li, Anna S., Jack F. Ingham, and Rachel Lennon. "Genetic Disorders of the Glomerular Filtration Barrier." Clinical Journal of the American Society of Nephrology 15, no. 12 (2020): 1818–28. http://dx.doi.org/10.2215/cjn.11440919.

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The glomerular filtration barrier is a highly specialized capillary wall comprising fenestrated endothelial cells, podocytes, and an intervening basement membrane. In glomerular disease, this barrier loses functional integrity, allowing the passage of macromolecules and cells, and there are associated changes in both cell morphology and the extracellular matrix. Over the past 3 decades, there has been a transformation in our understanding about glomerular disease, fueled by genetic discovery, and this is leading to exciting advances in our knowledge about glomerular biology and pathophysiology

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Khalil, Ramzi, Reshma A. Lalai, Malgorzata I. Wiweger, et al. "Glomerular permeability is not affected by heparan sulfate glycosaminoglycan deficiency in zebrafish embryos." American Journal of Physiology-Renal Physiology 317, no. 5 (2019): F1211—F1216. http://dx.doi.org/10.1152/ajprenal.00126.2019.

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Proteinuria develops when specific components in the glomerular filtration barrier have impaired function. Although the precise components involved in maintaining this barrier have not been fully identified, heparan sulfate proteoglycans are believed to play an essential role in maintaining glomerular filtration. Although in situ studies have shown that a loss of heparan sulfate glycosaminoglycans increases the permeability of the glomerular filtration barrier, recent studies using experimental models have shown that podocyte-specific deletion of heparan sulfate glycosaminoglycan assembly does

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Charba, Deane S., Roger C. Wiggins, Meera Goyal, et al. "Antibodies to protein tyrosine phosphatase receptor type O (PTPro) increase glomerular albumin permeability (Palb)." American Journal of Physiology-Renal Physiology 297, no. 1 (2009): F138—F144. http://dx.doi.org/10.1152/ajprenal.00122.2008.

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Glomerular capillary filtration barrier characteristics are determined in part by the slit-pore junctions of glomerular podocytes. Protein tyrosine phosphatase receptor-O (PTPro) is a transmembrane protein expressed on the apical surface of podocyte foot processes. Tyrosine phosphorylation of podocyte proteins including nephrin may control the filtration barrier. To determine whether PTPro activity is required to maintain glomerular macromolecular permeability, albumin permeability ( Palb) was studied after incubation of glomeruli from normal animals with a series of monoclonal (mAb) and polyc

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Menon, Madhav C., Peter Y. Chuang, and Cijiang John He. "The Glomerular Filtration Barrier: Components and Crosstalk." International Journal of Nephrology 2012 (2012): 1–9. http://dx.doi.org/10.1155/2012/749010.

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The glomerular filtration barrier is a highly specialized blood filtration interface that displays a high conductance to small and midsized solutes in plasma but retains relative impermeability to macromolecules. Its integrity is maintained by physicochemical and signalling interplay among its three core constituents—the glomerular endothelial cell, the basement membrane and visceral epithelial cell (podocyte). Understanding the pathomechanisms of inherited and acquired human diseases as well as experimental injury models of this barrier have helped to unravel this interdependence. Key among t

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Dissertations / Theses on the topic "Glomerular Filtration Barrier"

1

Slater, Sadie. "Engineering the Glomerular Filtration Barrier in Vitro." Thesis, University of Bristol, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.499937.

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Azadi, Azin. "A 'dynamic' tissue model of glomerular filtration barrier maintenance, adaptation and potential pathways to failure." Thesis, Azadi, Azin (2022) A 'dynamic' tissue model of glomerular filtration barrier maintenance, adaptation and potential pathways to failure. PhD thesis, Murdoch University, 2022. https://researchrepository.murdoch.edu.au/id/eprint/66252/.

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The glomerular filtration barrier (GFB), within the kidney, is known to act as a filter. It must work effectively over its lifespan, avoiding common filter problems such as clogging. Previous mathematical studies mostly just considered how the GFB acts as a size and charge selective barrier. In contrast, here the aim is how the GFB continues to work long-term, despite its environmental changes. The overarching hypothesis presented here is that the tissue is continuously renewing, as podocyte-synthesized molecules are transported ‘upstream’ against the filtrate across the glomerular basement me

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Books on the topic "Glomerular Filtration Barrier"

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Elger, Marlies, and Wilhelm Kriz. The renal glomerulus. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0043.

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The glomerulus performs its functions with three major cell types. Endothelial cells and visceral epithelial cells (podocytes) lie on the inside and outside of the glomerular basement membrane, and together these three structures form the glomerular filtration barrier. Mesangial cells sit in the axial region. Pathologies of all these regions and cell types can be identified. Parietal epithelial cells lining Bowman’s capsule participate in crescent formation, and at the tubular pole some of these cells seem to represent a stem cell population for tubular cells and podocytes. The extraglomerular

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Saleem, Moin A., and Corinne Antignac. Molecular basis of nephrotic syndrome. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0327_update_001.

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Nephrotic syndrome is broadly a disorder of the glomerular filtration barrier, but in practice the site of dysfunction in the great majority of pathologies is in the podocyte. Genetic causes of nephrotic syndrome provide the strongest proof of this. Almost all the genetic associations with nephrotic syndrome are podocyte proteins. Some basement membrane protein mutations associated with nephrotic syndrome may act through signalling to podocytes, or by causing severe disruption to their environment.

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Niaudet, Patrick, and Alain Meyrier. Minimal change disease. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0055_update_001.

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Minimal change disease is the most common cause of nephrotic syndrome in childhood but is not rare in adults. The factors altering permeability of the glomerular filtration barrier are not known, but podocyte structure is significantly altered in the condition and it seems certain that this cell is the target of whatever factors are responsible for the condition. It is still not clear that it is immunologically mediated and many of the agents used to treat it have direct effects on the podocyte. The differential diagnosis includes any other disease causing nephrotic syndrome, and a renal biops

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4

Hannover, Universität, ed. Role of size, charge and conformation of dissolved molecules and of fixed charges of the filtration barrier in glomerular permselectivity. Studies in the perfused-fixed rat kidney model: Einfluss von Grösse, Landung und Konformation gelöster Moleküle und fixierter Landungen der Filtrationsbarriere auf die Permselektivität des Glomerulus. Studien am Modell der isolierten, fixierten Niere. 1999.

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Book chapters on the topic "Glomerular Filtration Barrier"

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Perin, Laura, and Stefano Da Sacco. "Generation of a Glomerular Filtration Barrier on a Glomerulus-on-a-Chip Platform." In Methods in Molecular Biology. Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1693-2_8.

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Sopel, Nina, and Janina Müller-Deile. "Zebrafish Model to Study Podocyte Function Within the Glomerular Filtration Barrier." In Methods in Molecular Biology. Springer US, 2023. http://dx.doi.org/10.1007/978-1-0716-3179-9_11.

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Silverman, Melvin. "Studies of the Glomerular Filtration Barrier: Integration of Physiologic and Cell Biologic Experimental Approaches." In Whole Organ Approaches to Cellular Metabolism. Springer New York, 1998. http://dx.doi.org/10.1007/978-1-4612-2184-5_5.

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Oddsson, Á., J. Patrakka, and K. Tryggvason. "Glomerular Filtration Barrier." In Reference Module in Biomedical Sciences. Elsevier, 2014. http://dx.doi.org/10.1016/b978-0-12-801238-3.00201-4.

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Jalanko, Hannu, Christer Holmberg, and Karl Tryggvason. "Diseases of the Glomerular Filtration Barrier." In The Kidney. Elsevier, 2003. http://dx.doi.org/10.1016/b978-012722441-1/50029-4.

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de Souza, Diogo Benchimol, Bianca Martins Gregório, Marlene Benchimol, and Fernanda Amorim de Morais Nascimento. "Evaluation of the Glomerular Filtration Barrier by Electron Microscopy." In Modern Electron Microscopy in Physical and Life Sciences. InTech, 2016. http://dx.doi.org/10.5772/61811.

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7

Alejandro Tavera Díaz, Maiko, David Andrés Ballesteros Castro, Omar Lafuente Covarrubias, Alison Vannia Nava Rojas, and Israel Danny Rivas Salazar. "Recurrent Focal Segmental Glomerulosclerosis Post Renal Transplantation." In Advances in Kidney Transplantation [Working Title]. IntechOpen, 2025. https://doi.org/10.5772/intechopen.1006530.

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Focal segmental glomerulosclerosis (FSGS) is a major cause of nephrotic syndrome in children and adults, presenting a significant clinical challenge due to its high post-transplant recurrence rate and its negative impact on graft survival. The pathophysiology of recurrent FSGS (rFSGS) involves a complex interplay between circulating permeability factors and podocyte signaling pathways, leading to actin cytoskeleton disorganization and glomerular filtration barrier dysfunction. This review explores the epidemiology, risk factors, and pathogenic mechanisms of rFSGS, focusing on the central role

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Conference papers on the topic "Glomerular Filtration Barrier"

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Azeloglu, Evren U., Mark Stothers, Thomas J. Deerinck, et al. "3-D Quantitative Microanatomy of Rat Kidney Podocytes as Determined by Serial Block-Face Scanning Electron Microscopy." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80650.

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The shape of a cell is critical for proper signaling and resultant biological function [1]. Podocytes, kidney visceral epithelial cells, have a distinctive morphology with interdigitating foot processes that wrap around the capillaries of the glomeruli and, together with endothelial cells and the basement membrane, form the glomerular filtration barrier. In addition to forming the filtration barrier, slit diaphragms that connect the alternating foot processes from two podocytes are thought to be signaling hubs that regulate cell morphology and function.

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