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The Molecular Interactions between Filtered Proteins and Proximal Tubular Cells in Proteinuria
Author(s) -
Richard Baines,
Nigel J. Brunskill
Publication year - 2008
Publication title -
nephron. experimental nephrology
Language(s) - English
Resource type - Journals
ISSN - 1660-2129
DOI - 10.1159/000161982
Subject(s) - receptor , medicine , endocrinology , endocytosis , microbiology and biotechnology , inflammation , podocyte , epithelium , scavenger receptor , proteinuria , albumin , biology , kidney , chemistry , lipoprotein , genetics , cholesterol
Proteinuria is associated with progressive chronic kidney disease and poor cardiovascular outcomes. Exposure of proximal tubular epithelial cells to excess proteins leads to the development of proteinuric nephropathy with tubular atrophy, interstitial inflammation and scarring. Numerous signalling pathways are activated in proximal tubular epithelial cells under proteinuric conditions resulting in gene transcription, altered growth and the secretion of inflammatory and profibrotic mediators. Megalin, the proximal tubular scavenger receptor for filtered macromolecules, has intrinsic signalling functions and may also link albumin to growth factor receptor signalling via regulated intramembrane proteolysis. It now seems that endocytosis is not always a prerequisite for albumin-evoked alterations in proximal tubular cell phenotype. Recent evidence shows the presence of other potential receptors for proteins, such as the neonatal Fc receptor and CD36, in the proximal tubular epithelium.

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