Abstract
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.
Highlights
Tenofovir is recommended as a first-line therapy in HIV treatment
We investigated whether NF-B inflammatory signaling pathway plays a role in tenofovir nephrotoxicity
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Summary
Tenofovir is recommended as a first-line therapy in HIV treatment. 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 NF-B, a key transcription factor, which is known to mediate inflammation.The NF-B response proinflammatory genes include iNOS, COX, TNFa, and others such as PARP-1. We investigated whether NF-B inflammatory signaling pathway plays a role in tenofovir nephrotoxicity. Statistically significant increase in the mRNA and protein expressions of NFkB, and its target proinflammatory genes, iNOS, COX-2, TNF a and PARP-1 as compared with control
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