{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,19]],"date-time":"2026-09-19T20:08:58Z","timestamp":1789848538787,"version":"4.0.1"},"reference-count":53,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2026,3,13]],"date-time":"2026-03-13T00:00:00Z","timestamp":1773360000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,3,13]],"date-time":"2026-03-13T00:00:00Z","timestamp":1773360000000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["physoc.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Experimental Physiology"],"published-print":{"date-parts":[[2026,4]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Cardiosphere\u2010derived cells (CDCs) are a promising in vitro model for studying myocardial ischaemia\u2013reperfusion (I\u2013R) injury and testing potential therapeutic interventions. This study investigated the suitability of CDCs as a model for myocardial infarction (MI) and the effects of prolyl hydroxylase inhibitor (PHI) administration during reperfusion. CDCs were generated from neonatal mouse hearts and characterized by immunofluorescence, revealing a heterogeneous mixture of cardiomyocytes, smooth muscle cells, endothelial cells, and stem cells. The CDCs were subjected to oxygen\u2013glucose deprivation (OGD) followed by reperfusion with or without the PHI dimethyloxalylglycine (DMOG). Cell viability, hypoxia\u2010inducible factor 1\u2010alpha (HIF\u20101\u03b1) accumulation, and gene expression were analysed. The results showed that DMOG administration during reperfusion reduced lactate dehydrogenase release, indicating decreased cell death. HIF\u20101\u03b1 protein levels increased during OGD and were further stabilized by DMOG during reperfusion. The expression of HIF\u20101\u03b1 target genes, such as vascular endothelial growth factor (\n                    <jats:italic>Vegfa<\/jats:italic>\n                    ), and genes involved in regeneration and cardiac function, including connective tissue growth factor (\n                    <jats:italic>Ctgf<\/jats:italic>\n                    ), cyclin D2 (\n                    <jats:italic>Ccnd2<\/jats:italic>\n                    ), and beta\u20101 adrenergic receptor (\n                    <jats:italic>Adrb1<\/jats:italic>\n                    ), was modulated by OGD and DMOG treatment. Comparisons with an in vivo mouse I\u2013R injury model revealed similarities in gene expression patterns. In conclusion, CDCs serve as an effective in vitro model for studying I\u2013R injury, closely resembling the in vivo situation. Furthermore, PHI administration during reperfusion reduces cell death and modulates the expression of genes involved in cardioprotection and regeneration, highlighting the potential of PHIs as a therapeutic strategy for I\u2013R injury.\n                  <\/jats:p>","DOI":"10.1113\/ep093391","type":"journal-article","created":{"date-parts":[[2026,3,13]],"date-time":"2026-03-13T14:27:57Z","timestamp":1773412077000},"page":"2058-2072","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Cardioprotective effects of prolyl hydroxylase inhibitors during reperfusion in myocardial infarction: A study using cardiosphere\u2010derived cells"],"prefix":"10.1113","volume":"111","author":[{"given":"Luca","family":"Salh\u00f6fer","sequence":"first","affiliation":[{"name":"Institute of Physiology University Duisburg\u2010Essen  Essen Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ulrike B.","family":"Hendgen\u2010Cotta","sequence":"additional","affiliation":[{"name":"Department of Cardiology and Vascular Medicine, West German Heart and Vascular Centre, Medical Faculty University of Duisburg\u2010Essen  Essen Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9585-0531","authenticated-orcid":false,"given":"Joachim","family":"Fandrey","sequence":"additional","affiliation":[{"name":"Institute of Physiology University Duisburg\u2010Essen  Essen Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6848-3158","authenticated-orcid":false,"given":"Timm","family":"Schreiber","sequence":"additional","affiliation":[{"name":"Institute of Physiology and Pathophysiology, and Centre for Biomedical Education and Research (ZBAF) University of Witten\/Herdecke  Witten Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tristan","family":"Leu","sequence":"additional","affiliation":[{"name":"Institute of Physiology University Duisburg\u2010Essen  Essen Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2026,3,13]]},"reference":[{"key":"e_1_2_10_2_1","doi-asserted-by":"publisher","DOI":"10.1097\/FJC.0b013e3181e2bfef"},{"issue":"20","key":"e_1_2_10_3_1","article-title":"Stress response protein GJA1\u201020k promotes mitochondrial biogenesis, metabolic quiescence, and cardioprotection against ischemia\/reperfusion injury","volume":"3","author":"Basheer W. 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