APOL1 renal risk variants exacerbate podocyte injury by increasing inflammatory stress.

Hidefumi WakashinJurgen HeymannHila RoshanravanParnaz DaneshpajouhnejadAvi RosenbergMyung Kyun ShinMaarten HoekJeffrey B Kopp

Published in: BMC nephrology (2020)

These results suggest a possible mechanism for podocyte injury by which one of the APOL1 protein isoforms, APOL1-B3 and its renal risk variants, enhances inflammatory signaling.

Keyphrases

copy number
oxidative stress
small molecule
amino acid
heat stress