{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,26]],"date-time":"2026-10-26T11:35:53Z","timestamp":1793014553558,"version":"4.5.0"},"reference-count":36,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2026,10,16]],"date-time":"2026-10-16T00:00:00Z","timestamp":1792108800000},"content-version":"vor","delay-in-days":15,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"},{"start":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T00:00:00Z","timestamp":1790812800000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The Journal of Gene Medicine"],"published-print":{"date-parts":[[2026,10]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Atherosclerosis (AS) underlies a substantial proportion of cardiovascular morbidity and mortality, yet the molecular events that drive vascular cell injury remain only partly resolved.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We first compared aortic transcriptomes from apolipoprotein E\u2010deficient (ApoE\u2212\/\u2212) mice maintained on control or high\u2010fat diets. Candidate\u2010gene effects were then examined in human vascular smooth muscle cells (HVSMCs) challenged with oxidized low\u2010density lipoprotein (ox\u2010LDL).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>The aortic dataset contained 2832 differentially expressed genes (1800 increased and 1032 decreased). Of the five genes taken forward, ATP6V0D2 displayed a graded increase as the ox\u2010LDL concentration rose. Network and enrichment results connected ATP6V0D2 to proton movement, acidification of intracellular organelles, and iron transport. Silencing ATP6V0D2 limited the ox\u2010LDL\u2010evoked accumulation of neutral lipid and restrained cell\u2010cycle entry, motility, and invasion. At the molecular level, knockdown lowered acyl\u2010CoA synthetase long\u2010chain family member 4 (ACSL4) and recovered solute carrier family 7 member 11 (SLC7A11) and glutathione peroxidase 4 (GPX4). It also raised glutathione (GSH) abundance and superoxide dismutase (SOD) activity while decreasing malondialdehyde (MDA), reactive oxygen species (ROS), mitochondrial contraction, and cristae damage. Ferrostatin\u20101 shifted the molecular, redox, and ultrastructural readouts in the same direction.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>These data identify ATP6V0D2 as a contributor to the abnormal HVSMC phenotypes produced by ox\u2010LDL. Its depletion appears to blunt this response, in part through attenuation of changes compatible with ferroptosis and warrants further evaluation as a mechanistic target for AS.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/jgm.70113","type":"journal-article","created":{"date-parts":[[2026,10,17]],"date-time":"2026-10-17T00:32:14Z","timestamp":1792197134000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["ATP6V0D2 Promotes Atherosclerosis\u2010Associated Vascular Smooth Muscle Cell Dysfunction by Modulating Ferroptosis\u2010Related Signaling"],"prefix":"10.1002","volume":"28","author":[{"given":"Chaohui","family":"Zhang","sequence":"first","affiliation":[{"name":"Department of Cardiology The Second Affiliated Hospital of Anhui Medical University  Hefei Anhui 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