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    <datestamp>2026-04-08T12:09:42Z</datestamp>
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  <dc:date>2026-04-08</dc:date>
  <dc:title>Figure 1 Schematic overview of common mechanisms of DILI</dc:title>
  <dc:identifier>doi:10.57760/sciencedb.xbyxb.00139</dc:identifier>
  <dc:language>en</dc:language>
  <dc:description>Drugs are metabolized in the liver to generate reactive metabolites, which GSH and increase ROS, thereby triggering oxidative stress. This is followed by mitochondrial dysfunction-characterized by ATP depletion, opening of the PTP and/or MOMP, Cyt c release, and activation of the caspase cascade-ultimately leading to cell death. In addition, some drugs inhibit transporters such as the BSEP, causing intracellular bile acid accumulation and cholestatic toxicity. Meanwhile, drug-protein adducts and DAMP activate inflammatory and immune responses, promoting immune cell recruitment and exacerbating hepatocellular injury.</dc:description>
  <dc:subject>drug-induced liver injury; western medicine; traditional Chinese medicine; acute liver failure; diagnostic biomarkers; genetic susceptibility; individualized pharmacotherapy</dc:subject>
  <dc:creator>DONG Jinrui</dc:creator>
  <dc:rights>PUBLIC</dc:rights>
  <dc:rights>https://creativecommons.org/licenses/by-nc-nd/4.0/</dc:rights>
  <dc:type>dataset</dc:type>
  <dc:publisher>Science Data Bank</dc:publisher>
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