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Figure 8
Summary figure.
Based on the data acquired in this study, we posit that CLVS1 function is required for CME in podocytes and disruptions in this process lead to disruption of GFB resulting in glomerular disease. The p.H310Y variant reduces the CME of key podocyte molecules, such as α-tocopherol, whose absence drives increased ROS and reduces viability. This pathological condition can be improved by the increased macropinocytosis and antioxidant enzyme activity in podocytes caused by corticosteroid treatment.
Acknowledgments
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