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 Pozzi. PI3-kinase and TGF-β in glomerular nephropathy: which comes first? Kidney international. 2012 Sep;82(5):507-9
PMID: 22892855
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