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                    <forename type="first">María</forename>
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                <title level="j">Cell Reports Medicine</title>
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                  <publisher>Cell Press</publisher>
                  <biblScope unit="volume">5</biblScope>
                  <biblScope unit="issue">7</biblScope>
                  <biblScope unit="pp">101653</biblScope>
                  <date type="datePub">2024-07</date>
                  <date type="dateEpub">2024-07-16</date>
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                <term xml:lang="en">necrosis</term>
                <term xml:lang="en">mitochondria</term>
                <term xml:lang="en">NEDD8</term>
                <term xml:lang="en">APAP</term>
                <term xml:lang="en">DILI</term>
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              <p>Drug-induced liver injury (DILI) is a significant cause of acute liver failure (ALF) and liver transplantation in the Western world. Acetaminophen (APAP) overdose is a main contributor of DILI, leading to hepatocyte cell death through necrosis. Here, we identified that neddylation, an essential post-translational modification involved in the mitochondria function, was upregulated in liver biopsies from patients with APAP-induced liver injury (AILI) and in mice treated with an APAP overdose. MLN4924, an inhibitor of the neuronal precursor cell-expressed developmentally downregulated protein 8 (NEDD8)-activating enzyme (NAE-1), ameliorated necrosis and boosted liver regeneration in AILI. To understand how neddylation interferes in AILI, whole-body biotinylated NEDD8 (bioNEDD8) and ubiquitin (bioUB) transgenic mice were investigated under APAP overdose with and without MLN4924. The cytidine diphosphate diacylglycerol (CDP-DAG) synthase TAM41, responsible for producing cardiolipin essential for mitochondrial activity, was found modulated under AILI and restored its levels by inhibiting neddylation. Understanding this ubiquitin-like crosstalk in AILI is essential for developing promising targeted inhibitors for DILI treatment.</p>
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