ArticleAmerican journal of physiology. Renal physiology2011
Dystroglycan does not contribute significantly to kidney development or function, in health or after injury.
Article in American journal of physiology. Renal physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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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Who cites it
27 citing papers in PubMed, 38 citations in OpenAlex.
- Proteomic Insights into the Maladaptive Biology of Steroid-Resistant Nephrotic Syndrome.Kidney international reports · 2026Article
- Glomerular basement membrane structural integrity dictates trans-tissue deposition of laminin in the kidney.Cell reports · 2026Article
- Laminin Receptors in Peripheral Tissues: Functions Revealed by Analysis of Knockout Mice.The American journal of pathology · 2025Review
- Suppression of dystroglycan function accompanies pancreatic acinar-to-ductal metaplasia and favours dysplasia development.The Journal of pathology · 2024Article
- The microstructure of laminin-111 compensates for dystroglycan loss in mammary epithelial cells in downstream expression of milk proteins.Biomaterials · 2019Article
- Extracellular Matrix in Kidney Fibrosis: More Than Just a Scaffold.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2019Review
- Basement Membrane Defects in Genetic Kidney Diseases.Frontiers in pediatrics · 2018Review
- Rethinking glomerular basement membrane thickening in diabetic nephropathy: adaptive or pathogenic?American journal of physiology. Renal physiology · 2016Review
- Podocyte-actin dynamics in health and disease.Nature reviews. Nephrology · 2016Review
- Cells of renin lineage are adult pluripotent progenitors in experimental glomerular disease.American journal of physiology. Renal physiology · 2015Article
- ACE-inhibition increases podocyte number in experimental glomerular disease independent of proliferation.Journal of the renin-angiotensin-aldosterone system : JRAAS · 2015Article
- Genetic Engineering of Dystroglycan in Animal Models of Muscular Dystrophy.BioMed research international · 2015Review
- Cell Receptor-Basement Membrane Interactions in Health and Disease: A Kidney-Centric View.Current topics in membranes · 2015Review
- Endogenous glucuronyltransferase activity of LARGE or LARGE2 required for functional modification of α-dystroglycan in cells and tissues.The Journal of biological chemistry · 2014Article
- Cells of renin lineage take on a podocyte phenotype in aging nephropathy.American journal of physiology. Renal physiology · 2014Article
- The importance of podocyte adhesion for a healthy glomerulus.Frontiers in endocrinology · 2014Review
- Cells of renin lineage are progenitors of podocytes and parietal epithelial cells in experimental glomerular disease.The American journal of pathology · 2013Article
- The glomerular basement membrane as a barrier to albumin.Nature reviews. Nephrology · 2013Review
- Cell-matrix adhesion of podocytes in physiology and disease.Nature reviews. Nephrology · 2013Review
- Loss of LARGE2 disrupts functional glycosylation of α-dystroglycan in prostate cancer.The Journal of biological chemistry · 2013Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Dystroglycan (DG or DAG1) is considered a critical link between the basement membrane and the cytoskeleton in multiple tissues. DG consists of two subunits, an extracellular α-subunit that binds laminin and other basement membrane components, and a transmembrane β-subunit. DG-null mouse embryos die during early embryogenesis because DG is required for Reichert's membrane formation. DG also forms an integral part of the dystrophin-glycoprotein complex in muscle. Although no human DG mutations have been reported, multiple forms of muscular dystrophy have been linked to DG glycosylation defects, and targeted deletion of muscle DG causes muscular dystrophy in mice. Moreover, DG is widely distributed in endothelial and epithelial cells, including those in the kidney. There has therefore been significant interest in DG's role in the kidney, especially in podocytes. Previous reports suggested that DG's disturbance in podocytes might cause glomerular filtration barrier abnormalities. To fully understand DG's contribution to nephrogenesis and kidney function, we used a conditional DG allele and a variety of Cre mice to systematically delete DG from podocytes, ureteric bud, metanephric mesenchyme, and then from the whole kidney. Surprisingly, none of these conditional deletions resulted in significant morphological or functional abnormalities in the kidney. Furthermore, DG-deficient podocytes did not show increased susceptibility to injury, and DG-deficient kidneys did not show delayed recovery. Integrins are therefore likely the primary extracellular matrix receptors in renal epithelia.
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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.