<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>241(8)</volume><submitter>Heuschkel MA</submitter><funding>Deutsche Forschungsgemeinschaft</funding><funding>Horizon 2020 Framework Programme</funding><funding>Deutsche Herzstiftung</funding><pubmed_abstract>&lt;h4>Aim&lt;/h4>Vascular calcification (VC), a characteristic feature of peripheral artery disease in patients with diabetes and chronic kidney disease, has been associated with poor prognosis. We hypothesize that hyperglycemia drives VC through alterations in metabolomic and transcriptomic profiles.&lt;h4>Methods&lt;/h4>Human coronary artery smooth muscle cells (SMCs) were cultured with 0, 5.5, and 25 mM glucose under calcifying conditions. Untargeted metabolomic and transcriptomic analyses were performed at different time points. Mitochondrial respiration was examined using Seahorse analysis.&lt;h4>Results&lt;/h4>Glucose-treated SMCs promoted extracellular matrix (ECM) calcification in a concentration- and time-dependent manner. The absence of glucose entirely abolished SMC calcification but reduced SMC</pubmed_abstract><journal>Acta physiologica (Oxford, England)</journal><pagination>e70075</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12230643</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Hypotaurine Reduces Glucose-Mediated Vascular Calcification.</pubmed_title><pmcid>PMC12230643</pmcid><pubmed_authors>Heuschkel MA</pubmed_authors><pubmed_authors>Schurgers L</pubmed_authors><pubmed_authors>Adamski J</pubmed_authors><pubmed_authors>Jahnen-Dechent W</pubmed_authors><pubmed_authors>Artati A</pubmed_authors><pubmed_authors>Goettsch C</pubmed_authors><pubmed_authors>Graber S</pubmed_authors><pubmed_authors>Marx N</pubmed_authors><pubmed_authors>Jaminon A</pubmed_authors><pubmed_authors>Jankowski J</pubmed_authors></additional><is_claimable>false</is_claimable><name>Hypotaurine Reduces Glucose-Mediated Vascular Calcification.</name><description>&lt;h4>Aim&lt;/h4>Vascular calcification (VC), a characteristic feature of peripheral artery disease in patients with diabetes and chronic kidney disease, has been associated with poor prognosis. We hypothesize that hyperglycemia drives VC through alterations in metabolomic and transcriptomic profiles.&lt;h4>Methods&lt;/h4>Human coronary artery smooth muscle cells (SMCs) were cultured with 0, 5.5, and 25 mM glucose under calcifying conditions. Untargeted metabolomic and transcriptomic analyses were performed at different time points. Mitochondrial respiration was examined using Seahorse analysis.&lt;h4>Results&lt;/h4>Glucose-treated SMCs promoted extracellular matrix (ECM) calcification in a concentration- and time-dependent manner. The absence of glucose entirely abolished SMC calcification but reduced SMC</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Aug</publication><modification>2026-07-15T09:02:35.924Z</modification><creation>2026-07-02T03:08:56.011Z</creation></dates><accession>S-EPMC12230643</accession><cross_references><pubmed>40620033</pubmed><doi>10.1111/apha.70075</doi></cross_references></HashMap>