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        <datestamp>2026-09-30T04:04:01Z</datestamp>
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        <oai_dc:dc xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance"  xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xmlns:dc="http://purl.org/dc/elements/1.1/" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd">
          <dc:title>Quercetin Alleviates
TMT-Induced PANoptosis in Chicken
Skeletal Muscle through Modulation of the ROS/mtDNA Axis</dc:title>
          <dc:creator>Chengguo Liu (2745184)</dc:creator>
          <dc:creator>Ping Zhang (86495)</dc:creator>
          <dc:creator>Yue Zhai (3141960)</dc:creator>
          <dc:creator>Fangfang Wu (526041)</dc:creator>
          <dc:creator>Jiahui Duan (9284688)</dc:creator>
          <dc:creator>Tong Xu (762586)</dc:creator>
          <dc:creator>Lixia Zhao (174165)</dc:creator>
          <dc:subject>Biophysics</dc:subject>
          <dc:subject>Biochemistry</dc:subject>
          <dc:subject>Medicine</dc:subject>
          <dc:subject>Cell Biology</dc:subject>
          <dc:subject>Genetics</dc:subject>
          <dc:subject>Molecular Biology</dc:subject>
          <dc:subject>Physiology</dc:subject>
          <dc:subject>Biological Sciences not elsewhere classified</dc:subject>
          <dc:subject>Information Systems not elsewhere classified</dc:subject>
          <dc:subject>Inorganic Chemistry</dc:subject>
          <dc:subject>Infectious Diseases</dc:subject>
          <dc:subject>Computational  Biology</dc:subject>
          <dc:subject>respiratory chain dysfunction</dc:subject>
          <dc:subject>recognized systemic toxicity</dc:subject>
          <dc:subject>reactive oxygen species</dc:subject>
          <dc:subject>network analysis indicated</dc:subject>
          <dc:subject>restored mitochondrial homeostasis</dc:subject>
          <dc:subject>molecular dynamics simulations</dc:subject>
          <dc:subject>mitochondrial dynamic imbalance</dc:subject>
          <dc:subject>skeletal muscle effects</dc:subject>
          <dc:subject>chicken skeletal muscle</dc:subject>
          <dc:subject>associated muscle damage</dc:subject>
          <dc:subject>vitro validation showed</dc:subject>
          <dc:subject>environmental organotin contaminant</dc:subject>
          <dc:subject>mtdna axis trimethyltin</dc:subject>
          <dc:subject>quercetin alleviates tmt</dc:subject>
          <dc:subject>que alleviates tmt</dc:subject>
          <dc:subject>vitro validation</dc:subject>
          <dc:subject>muscle injury</dc:subject>
          <dc:subject>induced skeletal</dc:subject>
          <dc:subject>mtdna axis</dc:subject>
          <dc:subject>mitochondrial regulators</dc:subject>
          <dc:subject>mitochondrial dna</dc:subject>
          <dc:subject>associated proteins</dc:subject>
          <dc:subject>sensing pathways</dc:subject>
          <dc:subject>remain unclear</dc:subject>
          <dc:subject>related signaling</dc:subject>
          <dc:subject>protective mechanism</dc:subject>
          <dc:subject>oxidative stress</dc:subject>
          <dc:subject>molecular docking</dc:subject>
          <dc:subject>mediated protection</dc:subject>
          <dc:subject>feed additive</dc:subject>
          <dc:subject>dietary intervention</dc:subject>
          <dc:subject>cytosolic dna</dc:subject>
          <dc:description>Trimethyltin
(TMT) is an environmental organotin contaminant with
recognized systemic toxicity, but its skeletal muscle effects and
the protective mechanism of quercetin (Que) remain unclear. This study
integrated network toxicology, molecular docking, molecular dynamics
simulations, and in vivo/in vitro validation to investigate Que-mediated
protection against TMT-induced skeletal-muscle injury. Network analysis
indicated the involvement of oxidative stress and cytosolic DNA-sensing
pathways, while docking and dynamic simulations suggested stable interactions
between Que and mitochondrial regulators and PANoptosis-associated
proteins. In vivo and in vitro validation showed that TMT induced
skeletal muscle injury, reactive oxygen species (ROS) accumulation,
mitochondrial dynamic imbalance, respiratory chain dysfunction, mitochondrial
DNA (mtDNA) leakage, and PANoptosis activation. Que markedly suppressed
ROS generation, restored mitochondrial homeostasis, reduced cytosolic
mtDNA leakage, and inhibited PANoptosis-related signaling. Collectively,
Que alleviates TMT-induced skeletal muscle toxicity by regulating
the ROS/mtDNA axis, supporting its potential as a dietary intervention
or feed additive against organotin-associated muscle damage.</dc:description>
          <dc:date>2026-09-30T00:00:00Z</dc:date>
          <dc:type>Text</dc:type>
          <dc:type>Journal contribution</dc:type>
          <dc:identifier>10.1021/acs.jafc.6c06054.s001</dc:identifier>
          <dc:relation>https://figshare.com/articles/journal_contribution/Quercetin_Alleviates_TMT-Induced_PANoptosis_in_Chicken_Skeletal_Muscle_through_Modulation_of_the_ROS_mtDNA_Axis/34029337</dc:relation>
          <dc:rights>CC BY-NC 4.0</dc:rights>
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