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Hussain S et al. - The authors propose that disruption of the slit diaphragm leads to activation of NF-kB; subsequent upregulation of NF-kB-driven genes results in glomerular damage mediated by NF-kB-dependent pathways. Nephrin may normally limit NF-kB activity in the podocyte, suggesting a mechanism by which it might discourage the evolution of glomerular disease.

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