<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>11</volume><submitter>Yuan C</submitter><pubmed_abstract>&lt;h4>Objective&lt;/h4>Previous studies have shown that high glucose (HG) induces endothelial cell (EC) damage via endothelial-to-mesenchymal transition (EndMT). Although the underlying mechanisms are still unclear, recent studies have demonstrated the role of calcium-sensing receptor (CaSR) in mediating EC damage. Therefore, the aim of our study was to investigate whether CaSR mediates HG-induced EndMT and to determine the underlying mechanism.&lt;h4>Methods&lt;/h4>Bioinformatics analysis of microarray profiles (GSE30780) and protein-protein interaction (PPI) analyses were performed to select the hub genes. As for &lt;i>in vitro&lt;/i> research, the human aortic ECs (HAECs) were exposed to HG to induce EndMT. The expression of CaSR and β-catenin was determined, as well as their effects on EndMT (endotheli</pubmed_abstract><journal>Frontiers in physiology</journal><pagination>629542</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7844313</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Calcium-Sensing Receptor Participates in High Glucose-Induced EndMT in Primary Human Aortic Endothelial Cells.</pubmed_title><pmcid>PMC7844313</pmcid><pubmed_authors>Yang X</pubmed_authors><pubmed_authors>Yuan C</pubmed_authors><pubmed_authors>Ni L</pubmed_authors><pubmed_authors>Zhang C</pubmed_authors><pubmed_authors>Wu X</pubmed_authors></additional><is_claimable>false</is_claimable><name>Calcium-Sensing Receptor Participates in High Glucose-Induced EndMT in Primary Human Aortic Endothelial Cells.</name><description>&lt;h4>Objective&lt;/h4>Previous studies have shown that high glucose (HG) induces endothelial cell (EC) damage via endothelial-to-mesenchymal transition (EndMT). Although the underlying mechanisms are still unclear, recent studies have demonstrated the role of calcium-sensing receptor (CaSR) in mediating EC damage. Therefore, the aim of our study was to investigate whether CaSR mediates HG-induced EndMT and to determine the underlying mechanism.&lt;h4>Methods&lt;/h4>Bioinformatics analysis of microarray profiles (GSE30780) and protein-protein interaction (PPI) analyses were performed to select the hub genes. As for &lt;i>in vitro&lt;/i> research, the human aortic ECs (HAECs) were exposed to HG to induce EndMT. The expression of CaSR and β-catenin was determined, as well as their effects on EndMT (endotheli</description><dates><release>2020-01-01T00:00:00Z</release><publication>2020</publication><modification>2026-04-08T02:28:14.474Z</modification><creation>2021-02-21T05:27:07Z</creation></dates><accession>S-EPMC7844313</accession><cross_references><pubmed>33519531</pubmed><doi>10.3389/fphys.2020.629542</doi></cross_references></HashMap>