The endothelial glycocalyx (eGlx) constitutes the first barrier to protein in all blood vessels. This is particularly noteworthy in the renal glomerulus, an ultrafiltration barrier. Leakage of protein, such as albumin, across glomerular capillaries results in albumin in the urine (albuminuria). This is a hall mark of kidney disease and can reflect loss of blood vessel integrity in microvascular beds elsewhere. We discuss evidence demonstrating that targeted damage to the glomerular eGlx results in increased glomerular albumin permeability. EGlx is lost in diabetes and experimental models demonstrate loss from glomerular endothelial cells. Vascular endothelial growth factor (VEGF)A is upregulated in early diabetes, which is associated with albuminuria. Treatment with paracrine growth factors such as VEGFC, VEGF165b and angiopoietin-1 can modify VEGFA signalling, rescue albumin permeability and restore glomerular eGlx in models of diabetes. Manipulation of VEGF receptor 2 signalling, or a common eGlx biosynthesis pathway by these growth factors, may protect and restore the eGlx layer. This would help to direct future therapeutics in diabetic nephropathy.

中文翻译：

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糖尿病肾病中生长因子对内皮糖萼的修复作用。

内皮糖萼（eGlx）构成了所有血管中蛋白质的第一道屏障。这在肾小球超滤屏障中尤其值得注意。跨肾小球毛细血管的蛋白质（例如白蛋白）泄漏导致尿液中的白蛋白（白蛋白尿）。这是肾脏疾病的标志，可以反映其他地方微血管床中血管完整性的丧失。我们讨论的证据表明，对肾小球eGlx的靶向损伤会导致肾小球白蛋白通透性增加。EGlx在糖尿病中丢失，实验模型证明肾小球内皮细胞丢失。血管内皮生长因子（VEGF）A在早期糖尿病中被上调，这与蛋白尿有关。用旁分泌生长因子（例如VEGFC，在糖尿病模型中，VEGF165b和血管生成素-1可以修饰VEGFA信号传导，挽救白蛋白通透性并恢复肾小球eGlx。通过这些生长因子操纵VEGF受体2信号传导或常见的eGlx生物合成途径可以保护和恢复eGlx层。这将有助于指导糖尿病肾病的未来治疗。