Kidney Int. 2012 Sep;82(5):507-9. doi: 10.1038/ki.2012.154.
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.
转化生长因子-β (TGF-β) 和磷脂酰肌醇-3-激酶 (PI3K) 同工型有助于肾小球疾病。Finer 及其同事定义了通常由造血细胞表达的 PI3K 的 p110γ 催化同工型和 TGF-β 在阿霉素介导的肾小球损伤中的时间和选择性作用。足细胞早期异位上调 p110γ 驱动初始损伤和蛋白尿，而晚期 TGF-β 上调则驱动纤维化。因此，蛋白尿和肾纤维化分别涉及由 p110γ 和 TGF-β 激活的不同信号通路。
