PI3-kinase and TGF-β in glomerular nephropathy: which comes first?
Transforming growth factor-β (TGF-β) and phosphatidylinositol-3-kinase (PI3 K) isoforms contribute to glomerular disease. Finer and colleagues define a temporal and selective role for the p110γ catalytic isoform of PI3 K, normally expressed by hematopoietic cells, and TGF-β in adriamycin-mediated glomerular injury. Early ectopic upregulation of p110γ by podocytes drives initial injury and proteinuria, whereas late upregulation of TGF-β drives fibrogenesis. Thus, proteinuria and renal fibrogenesis involve distinct signaling activated by p110γ and TGF-β, respectively.
Ambra
A
Pozzi
D000818:Animals; D058534:Class I Phosphatidylinositol 3-Kinases / Q000378:metabolism*; D004317:Doxorubicin; D005923:Glomerulosclerosis, Focal Segmental / Q000201:enzymology*; D007668:Kidney / Q000201:enzymology*; D008297:Male; D011507:Proteinuria / Q000201:enzymology*; D015398:Signal Transduction; D051900:Smad3 Protein / Q000378:metabolism*
D051900:Smad3 Protein; C497791:Smad3 protein, mouse; D004317:Doxorubicin; C509622:1-phosphatidylinositol 3-kinase p110 subunit, mouse; D058534:Class I Phosphatidylinositol 3-Kinases