Coward Richard J M, Saleem Moin A
Academic and Children's Renal Unit, Southmead Hospital, Bristol, UK.
Curr Diabetes Rev. 2011 Jan;7(1):22-7. doi: 10.2174/157339911794273883.
Diabetic nephropathy (DN) presents with a gradual breakdown of the glomerular filtration barrier to protein, culminating in widespread glomerular damage and renal failure. The podocyte is the central cell of the glomerular filtration barrier, and possesses unique architectural and signaling properties guided by the expression of key podocyte specific proteins. How these cellular features are damaged by the diabetic milieu is unclear, but what is becoming increasingly clear is that damage to the podocyte is a central event in DN. Here we present accumulating evidence that insulin action itself is important in podocyte biology, and may be deranged in the pathomechanism of early DN. This introduces a rationale for therapeutic intervention to improve podocyte insulin sensitivity early in the presentation of DN.
糖尿病肾病（DN）表现为肾小球滤过屏障对蛋白质的逐渐破坏，最终导致广泛的肾小球损伤和肾衰竭。足细胞是肾小球滤过屏障的核心细胞，具有由关键足细胞特异性蛋白的表达所引导的独特结构和信号特性。目前尚不清楚这些细胞特征如何被糖尿病环境破坏，但越来越清楚的是，足细胞损伤是DN的核心事件。在此，我们提供越来越多的证据表明，胰岛素作用本身在足细胞生物学中很重要，并且可能在早期DN的发病机制中出现紊乱。这为在DN发病早期进行治疗干预以提高足细胞胰岛素敏感性提供了理论依据。
