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        <datestamp>2026-09-21T22:02:27Z</datestamp>
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          <dc:title>Table 1_Exploratory ferroptosis-related transcriptomic patterns in dilated cardiomyopathy and pan-cancer datasets with H9c2 RT-qPCR assessment.docx</dc:title>
          <dc:creator>Mingwei Yang (1778551)</dc:creator>
          <dc:creator>Huayin Li (795744)</dc:creator>
          <dc:creator>Fangchao Wang (24238959)</dc:creator>
          <dc:creator>Jiao Wang (47178)</dc:creator>
          <dc:creator>Boli Ran (25085815)</dc:creator>
          <dc:creator>Rui He (824726)</dc:creator>
          <dc:subject>Genetics</dc:subject>
          <dc:subject>bulk transcriptomics</dc:subject>
          <dc:subject>dilated cardiomyopathy</dc:subject>
          <dc:subject>ferroptosis</dc:subject>
          <dc:subject>hypertensive heart disease</dc:subject>
          <dc:subject>pan-cancer</dc:subject>
          <dc:subject>RT-qPCR</dc:subject>
          <dc:subject>single-cell RNA sequencing</dc:subject>
          <dc:description>Background and Aims&lt;p&gt;Ferroptosis-related pathways have been implicated in cardiovascular remodeling and cancer, but their relevance to hypertensive heart disease (HHD) remains uncertain. This study examined transcriptomic patterns in a dilated cardiomyopathy (DCM) dataset and used pan-cancer data only for descriptive context; it did not analyze primary HHD tissue.&lt;/p&gt;Methods&lt;p&gt;GSE183852 data were restricted to the explicitly identified non-diseased sample H_ZC-11-292 (8,749 cells) and DCM sample HDCM1 (7,202 cells). H_ZC-LVAD-1 was excluded because GEO metadata classify it as DCM. Full-rank cell-level Wilcoxon results were retained, with all single-cell tests treated as descriptive. GSE5406 groups were assigned from GEO sample titles (194 failing and 16 non-failing myocardium samples), and TCGA data were used for descriptive pan-cancer context. GPX4, SLC7A11, ACSL4, and TFRC mRNA were assessed by RT-qPCR in Ang II-stimulated H9c2 cells.&lt;/p&gt;Results&lt;p&gt;Fourteen cluster-derived cell categories were retained. Cardiomyocytes, macrophages, and endothelial cells were not detected in the selected DCM donor, so no condition-specific inference was made for those categories. Among 109 detected ferroptosis-related genes, 60 met the cell-level up threshold, 24 met the down threshold, and 25 were nonsignificant; these counts are not donor-level evidence. In GSE5406, 5 of 99 tested ferroptosis-related genes met |log2FC| &gt; 0.5 and BH-adjusted p &lt; 0.05. Fold changes for 96 detected genes were uncorrelated across platforms (r = 0.034, p = 0.740). RT-qPCR showed lower GPX4 and SLC7A11 and higher ACSL4 and TFRC mRNA, with gene- and context-specific directionality (Supplementary Table S1).&lt;/p&gt;Conclusion&lt;p&gt;The analyses identify exploratory, donor- and context-dependent transcriptional patterns. They do not establish ferroptosis as a causal mechanism, biomarker, or treatment target in primary HHD. Multi-donor disease-specific cohorts and protein-level and functional experiments are required.&lt;/p&gt;</dc:description>
          <dc:date>2026-09-21T22:02:27Z</dc:date>
          <dc:type>Dataset</dc:type>
          <dc:type>Dataset</dc:type>
          <dc:identifier>10.3389/fgene.2026.1909716.s001</dc:identifier>
          <dc:relation>https://figshare.com/articles/dataset/Table_1_Exploratory_ferroptosis-related_transcriptomic_patterns_in_dilated_cardiomyopathy_and_pan-cancer_datasets_with_H9c2_RT-qPCR_assessment_docx/33960121</dc:relation>
          <dc:rights>CC BY 4.0</dc:rights>
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