失去立足点： Rac1 信号导致足细胞脱离和 FSGS。
Losing their footing: Rac1 signaling causes podocyte detachment and FSGS.
机构信息
Division of Nephrology, Department of Medicine, Duke University and Durham VA Medical Centers, Durham, North Carolina, USA.
Division of Nephrology, Department of Medicine, Duke University and Durham VA Medical Centers, Durham, North Carolina, USA.
出版信息
Kidney Int. 2017 Aug;92(2):283-285. doi: 10.1016/j.kint.2017.03.045.
Selective modulation of Rho GTPase activity in podocytes recapitulates characteristic features of human nephrosis. Using a mouse model, Robins et al. found that high levels of Rac1 activation in podocytes caused podocyte detachment and glomerulosclerosis. Podocyte Rac1 activity was enhanced in biopsy specimens from patients with nephrosis, and serum from this patient population activated Rac1 in cultured podocytes. These data provide a causal link between podocyte Rac1 activation and human nephrotic diseases.
选择性调节足细胞中 Rho GTPase 的活性可重现人类肾病的特征。Robins 等人利用小鼠模型发现，足细胞中 Rac1 的高激活水平导致足细胞脱离和肾小球硬化。肾病患者的活检标本中足细胞 Rac1 活性增强，且来自该患者群体的血清可在培养的足细胞中激活 Rac1。这些数据为足细胞 Rac1 激活与人类肾病之间提供了因果关系。
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