Tenofovir induced renal damage is associated with activation of NF-κB inflammatory signaling pathway and PARP overactivation
نویسندگان
چکیده
Background Tenofovir is recommended as a first-line therapy in HIV treatment. However, its long term use is associated with proximal tubular injury and renal dysfunction. Tenofovir has been shown to target the proximal tubular mitochondria, resulting in severe mitochondrial injury and overproduction of ROS and RNS. ROS are potent stimuli for the activation of NFB, a key transcription factor, which is known to mediate inflammation.The NFB response proinflammatory genes include iNOS, COX, TNFa, and others such as PARP-1. In the present study, we investigated whether NFB inflammatory signaling pathway plays a role in tenofovir nephrotoxicity.
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