{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,19]],"date-time":"2026-10-19T21:16:11Z","timestamp":1792444571803,"version":"4.5.0"},"reference-count":49,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2022,9,2]],"date-time":"2022-09-02T00:00:00Z","timestamp":1662076800000},"content-version":"vor","delay-in-days":244,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82100287"],"award-info":[{"award-number":["82100287"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81570331"],"award-info":[{"award-number":["81570331"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Oxidative Medicine and Cellular Longevity"],"published-print":{"date-parts":[[2022,1]]},"abstract":"<jats:p>\n                    Cardiac microvascular endothelial cell ischemia\u2010reperfusion (CMEC I\/R) injury occurs in approximately 50% of acute myocardial infarction patients subjected to successful revascularization therapy. This injury leads to cardiac microcirculatory system dysfunctions, which seriously affect cardiac functions and long\u2010term prognostic outcomes. Previously, we elucidated the role of lysine\u2010specific demethylase 3A (KDM3A) in protecting cardiomyocytes from I\/R injury; however, its roles in CMEC I\/R injuries have yet to be fully established. In this study, hypoxia\/reoxygenation (H\/R) treatment significantly impaired CMEC functions and induced their pyroptosis, accompanied by KDM3A downregulation. Then, gain\u2010 and loss\u2010of\u2010function assays were performed to investigate the roles of KDM3A in CMEC H\/R injury\n                    <jats:italic>in vitro<\/jats:italic>\n                    . KDM3A knockout enhanced CMEC malfunctions and accelerated the expressions of pyroptosis\u2010associated proteins, such as NLRP3, cleaved\u2010caspase\u20101, ASC, IL\u20101\n                    <jats:italic>\u03b2<\/jats:italic>\n                    , GSDMD\u2010N, and IL\u201018. Conversely, KDM3A overexpression developed ameliorated alternations in CMEC H\/R injury.\n                    <jats:italic>In vivo<\/jats:italic>\n                    , KDM3A knockout resulted in the deterioration of cardiac functions and decreased the no\u2010reflow area as well as capillary density. Mechanistically, KDM3A activated the PI3K\/Akt signaling pathway and ameliorated I\/R\u2010mediated CMEC pyroptosis. In conclusion, KDM3A is a promising treatment target for alleviating CMEC I\/R injury.\n                  <\/jats:p>","DOI":"10.1155\/2022\/4622520","type":"journal-article","created":{"date-parts":[[2022,9,2]],"date-time":"2022-09-02T15:35:09Z","timestamp":1662132909000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":18,"title":["KDM3A Attenuates Myocardial Ischemic and Reperfusion Injury by Ameliorating Cardiac Microvascular Endothelial Cell 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