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        <identifier>oai:figshare.com:article/33903540</identifier>
        <datestamp>2026-09-17T17:25:43Z</datestamp>
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          <dc:title>&lt;p&gt;Raw data.&lt;/p&gt;</dc:title>
          <dc:creator>Yuan Ding (617135)</dc:creator>
          <dc:creator>Xiang Wang (127867)</dc:creator>
          <dc:creator>Shihua Zong (25037415)</dc:creator>
          <dc:creator>Qiong Wen (8087294)</dc:creator>
          <dc:creator>Luyang Zhang (5677079)</dc:creator>
          <dc:subject>Biophysics</dc:subject>
          <dc:subject>Cell Biology</dc:subject>
          <dc:subject>Genetics</dc:subject>
          <dc:subject>Neuroscience</dc:subject>
          <dc:subject>Physiology</dc:subject>
          <dc:subject>Pharmacology</dc:subject>
          <dc:subject>Ecology</dc:subject>
          <dc:subject>Immunology</dc:subject>
          <dc:subject>Biological Sciences not elsewhere classified</dc:subject>
          <dc:subject>normalizing dynamic balance</dc:subject>
          <dc:subject>mechanistic framework linking</dc:subject>
          <dc:subject>work highlights iq</dc:subject>
          <dc:subject>related chondrocyte impairment</dc:subject>
          <dc:subject>div &gt;&lt; p</dc:subject>
          <dc:subject>modifying therapies targeting</dc:subject>
          <dc:subject>iq binds</dc:subject>
          <dc:subject>chondrocyte anabolic</dc:subject>
          <dc:subject>stabilizing activities</dc:subject>
          <dc:subject>promising candidate</dc:subject>
          <dc:subject>overexpression abolishes</dc:subject>
          <dc:subject>oa ),</dc:subject>
          <dc:subject>mitigates pro</dc:subject>
          <dc:subject>key mediator</dc:subject>
          <dc:subject>high affinity</dc:subject>
          <dc:subject>coupling anti</dc:subject>
          <dc:subject>catabolic imbalance</dc:subject>
          <dc:subject>aberrant inflammation</dc:subject>
          <dc:description>&lt;div&gt;&lt;p&gt;Osteoarthritis (OA), a prevalent degenerative joint disorder, is driven by chondrocyte anabolic-catabolic imbalance, aberrant inflammation, and mitochondrial dysfunction. Disease-modifying therapies targeting these pathological processes remain scarce, limiting effective clinical intervention. Herein, we demonstrate an isoquercitrin (IQ)-based chondroprotective strategy that rectifies osteoarthritis-related chondrocyte impairment by targeting &lt;i&gt;AKT1&lt;/i&gt;. IQ first reverses IL-1β-induced chondrocyte proliferation arrest, shifts metabolic homeostasis toward anabolism, and mitigates pro-inflammatory responses. It simultaneously restores mitochondrial homeostasis by normalizing dynamic balance. Mechanistically, IQ binds to AKT1 with high affinity, and &lt;i&gt;AKT1&lt;/i&gt; overexpression abolishes its protective effects—confirming &lt;i&gt;AKT1&lt;/i&gt; as a key mediator. This approach re-establishes chondrocyte functional homeostasis by coupling anti-inflammatory, metabolic-regulatory, and mitochondrial-stabilizing activities. This work highlights IQ as a promising candidate for osteoarthritis intervention and provides a mechanistic framework linking &lt;i&gt;AKT1&lt;/i&gt; targeting to chondroprotection.&lt;/p&gt;&lt;/div&gt;</dc:description>
          <dc:date>2026-09-17T17:25:25Z</dc:date>
          <dc:type>Dataset</dc:type>
          <dc:type>Dataset</dc:type>
          <dc:identifier>10.1371/journal.pone.0357989.s014</dc:identifier>
          <dc:relation>https://figshare.com/articles/dataset/_p_Raw_data_p_/33903540</dc:relation>
          <dc:rights>CC BY 4.0</dc:rights>
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