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Unlike a 30-minute ischemia, a 60-minute ischemic period followed by 1 day of reperfusion decreases the mRNA levels of the basolateral transporters, Ntcp and Oatp (all isoforms), as well as those of the canalicular export transporters, Mrp2 and Bsep.193 This has been confirmed at the protein level for Mrp2.194 At least part of these transcriptional alterations may be due to the ROS-dependent hepatic inflammatory response, which leads to release of cholestatic, proinflammatory cytokines with capability to impair transporter expression at a transcriptional level.221 However, down-regulation of Mrp2 protein is more profound than that of mRNA, suggesting additional post-transcriptional mechanisms.194 Although the causes underlying the latter phenomenon are presently unknown, the early oxidative stress-induced transporter internalization, sustained with time, may lead to the delivery of the endocytosed transporters to the lysosomal compartment, followed by degradation, as was suggested to occur late in lipopolysaccharide-induced cholestasis222 and in obstructive cholestasis223 in rats

Furthermore, as a typical activator, ATP activates the NLRP3 inflammasome in macrophages, leading to caspase-1/GDSDMD-mediated pyroptosis (33)

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Mikuls TR, Duryee MJ, England BR, Anderson DR, Hearth-Holmes M, Su K, et al