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        <datestamp>2026-09-28T12:02:56Z</datestamp>
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          <dc:title>Table 2_Retinal organoid–based evaluation of icariin-loaded extracellular vesicles for hypoxia-induced retinal injury via mitochondrial modulation.docx</dc:title>
          <dc:creator>Mira Park (212785)</dc:creator>
          <dc:creator>Hyeoun Ji Kim (25122231)</dc:creator>
          <dc:creator>Yoon-Ha Go (25122234)</dc:creator>
          <dc:creator>Hey Jin Lee (10895992)</dc:creator>
          <dc:creator>Young Il Yang (10330761)</dc:creator>
          <dc:creator>Dong Hyuck Bae (19480891)</dc:creator>
          <dc:creator>Jong man Yoo (25122237)</dc:creator>
          <dc:creator>Helen Lew (9608661)</dc:creator>
          <dc:subject>Cell Biology</dc:subject>
          <dc:subject>extracellular vesicles (EVs)</dc:subject>
          <dc:subject>hypoxia</dc:subject>
          <dc:subject>icariin</dc:subject>
          <dc:subject>mitochondria</dc:subject>
          <dc:subject>retinal organoid</dc:subject>
          <dc:description>Background&lt;p&gt;Hypoxic injury is a critical pathological factor in various retinal degenerative diseases, leading to mitochondrial dysfunction and irreversible loss of retinal neurons. This study investigated the neuroprotective potential of Icariin-loaded extracellular vesicles (EV_ICA) using both R28 retinal progenitor cells and human embryonic stem cell (hESC)-derived retinal organoids.&lt;/p&gt;Methods&lt;p&gt;EV_ICA were isolated and characterized by morphology, EV marker expression, and zeta potential analysis. A CoCl&lt;sub&gt;2&lt;/sub&gt;-induced hypoxic injury model was established in R28 cells and hESC-derived retinal organoids to evaluate the therapeutic effects of EV_ICA. Gene and protein expression analyses, bulk RNA sequencing (RNA-seq), gene set enrichment analysis (GSEA), mitochondrial ROS measurements, and intracellular ATP assays were performed to assess neuroprotective efficacy and mitochondrial function.&lt;/p&gt;Results&lt;p&gt;EV_ICA exhibited typical spherical morphology, expressed standard EV markers, and showed a shift toward a less negative zeta potential compared to Naïve EV. In hypoxia-injured retinal models, EV_ICA significantly restored the expression of key retinal and neuroprotective markers, including Syntaxin12, NeuN, Vegf, Rbpms, Brn-3a, and Bdnf, while suppressing Hif-1α accumulation. Transcriptomic and GSEA analyses revealed that EV_ICA reactivated biological pathways associated with phototransduction, visual perception, and retinal development that were impaired under hypoxic conditions. Furthermore, EV_ICA improved mitochondrial homeostasis by up-regulating mitochondrial-related genes, reducing mitochondrial ROS accumulation, and recovering intracellular ATP production.&lt;/p&gt;Conclusion&lt;p&gt;These findings demonstrate that EV_ICA exerts neuroprotective effects by preserving mitochondrial quality control and restoring functional retinal gene programs under hypoxic stress. EV_ICA may therefore serve as a promising therapeutic candidate for hypoxia-related retinal degeneration and provide potential applications for cell-free regenerative medicine.&lt;/p&gt;</dc:description>
          <dc:date>2026-09-28T12:02:56Z</dc:date>
          <dc:type>Dataset</dc:type>
          <dc:type>Dataset</dc:type>
          <dc:identifier>10.3389/fcell.2026.1891491.s001</dc:identifier>
          <dc:relation>https://figshare.com/articles/dataset/Table_2_Retinal_organoid_based_evaluation_of_icariin-loaded_extracellular_vesicles_for_hypoxia-induced_retinal_injury_via_mitochondrial_modulation_docx/34013547</dc:relation>
          <dc:rights>CC BY 4.0</dc:rights>
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