Podocytes as a Target of Insulin
Podocytes as a Target of Insulin
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DOI：
10.2174/157339911794273883
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发表时间：
2011-01-01
影响因子：
3.3
通讯作者：
Saleem, Moin A.
中科院分区：
文献类型：
--
作者：
Coward, Richard J. M.;Saleem, Moin A.
糖尿病肾病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害和肾功能衰竭。足细胞是肾小球滤过屏障的中心细胞，具有独特的结构和信号特性，由关键的足细胞特异性蛋白的表达所指导。这些细胞特征是如何被糖尿病环境破坏的尚不清楚，但越来越清楚的是，足细胞受损是糖尿病肾病的中心事件。在这里，我们提出了越来越多的证据，表明胰岛素作用本身在足细胞生物学中是重要的，并可能在早期糖尿病肾病的发病机制中错乱。这为治疗干预在糖尿病肾病早期改善足细胞胰岛素敏感性提供了理论基础。
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.