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Experimental model examines nephrin trafficking in nephrotic syndrome, suggesting mechanisms of podocyte injury.
Nephrin is an essential protein expressed at the slit diaphragm of podocytes and plays a crucial role in maintaining the integrity of the glomerular filtration barrier. We previously developed a novel experimental autoimmune nephrotic syndrome mouse model resembling idiopathic nephrotic syndrome in humans, induced by immunization with Crb2, a slit diaphragm protein that interacts with Nephrin. While proper trafficking of Nephrin to the podocyte surface is critical for its function, and impaired Nephrin turnover contributes to podocyte injury, the mechanisms underlying Nephrin trafficking in this model remain unknown.
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SUZUKI et al. (2026) studied this question.
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