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postulated the role of indoxyl sulfate in the pathogenesis of renal anemia: indoxyl sulfate could stimulate oxidative stress and induce eryptosis through Organic Anion Transporter 2 (OAT2)- and NADPH oxidase-dependent, as well as GSH-independent mechanisms [257]

Initially, the pathogenesis of NASH was explained by the 2-hit hypothesis, where the first hit, hepatic triglyceride accumulation (steatosis), increases the livers susceptibility to injury from second hits, such as inflammatory cytokines, mitochondrial dysfunction, and oxidative stress [37,38]

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