Inflammatory proteolysis generates pathogenic APOL1 fragments with distinct intracellular toxicities in podocytes derived from children with HIV associated nephropathy.
APOL1 risk variants are the strongest genetic determinants of HIV-associated nephropathy (HIVAN), yet the mechanisms linking inflammation to APOL1-mediated podocyte injury remain poorly understood because authentic patient-derived human disease models are lacking. Using urine-derived podocytes established from children with HIVAN and endogenous APOL1 reporter cell lines derived from these cells,…
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