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        <datestamp>2026-09-30T04:54:47Z</datestamp>
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          <dc:title>Mechanisms of polymyxin-induced nephrotoxicity: An integrated systems pharmacology approach</dc:title>
          <dc:creator>Xinpeng Yao (18882573)</dc:creator>
          <dc:subject>Medical microbiology not elsewhere classified</dc:subject>
          <dc:subject>Toxicology (incl. clinical toxicology)</dc:subject>
          <dc:subject>Pharmacology and pharmaceutical sciences not elsewhere classified</dc:subject>
          <dc:subject>Polymyxins</dc:subject>
          <dc:subject>Nephrotoxicity</dc:subject>
          <dc:subject>Endoplasmic reticulum stress</dc:subject>
          <dc:subject>KEAP1-NRF2-HMOX1</dc:subject>
          <dc:subject>Proteomics</dc:subject>
          <dc:subject>Proximal tubular epithelial cells</dc:subject>
          <dc:description>Polymyxin antibiotics are important last-resort treatments for life-threatening infections caused by drug-resistant bacteria, but their use is limited by kidney toxicity. This thesis investigated how polymyxins damage kidney cells and why some cells may cope better with this stress than others. Using multiple models, this research discovered that polymyxins can disturb normal protein handling inside kidney tubular cells and trigger protective stress responses. These findings improve our understanding of why kidney injury occurs during polymyxin treatment and may facilitate the discovery of novel, safer antibiotics to combat the major global medical challenge due to antimicrobial resistance.&lt;p&gt;&lt;/p&gt;</dc:description>
          <dc:date>2026-09-30T04:54:47Z</dc:date>
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          <dc:identifier>10.26180/34029870.v1</dc:identifier>
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          <dc:rights>In Copyright</dc:rights>
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