{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,17]],"date-time":"2026-08-17T14:44:48Z","timestamp":1786977888497,"version":"build-2736575974"},"reference-count":41,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2019,1,6]],"date-time":"2019-01-06T00:00:00Z","timestamp":1546732800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81360287"],"award-info":[{"award-number":["81360287"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J of Cellular Biochemistry"],"published-print":{"date-parts":[[2019,4]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    N\u2010methyl\u2010D\u2010aspartate receptor (NMDAR) activity plays a key role in cerebral ischemia. Although NMDAR is also expressed in cardiomyocytes, little research has been performed on NMDAR activity in myocardial ischemia. Here, using an in vitro oxygen\u2010glucose deprivation (OGD) cardiomyocyte model, we evaluated the effects of NMDAR activity upon calcium influx, viability, apoptosis, and investigated the roles of several key mitogen\u2010activated protein kinases (MAPKs). Primary human neonatal cardiomyocytes were cultured under OGD conditions to mimic in vivo ischemic conditions. Enhancing NMDAR activity via NMDA significantly promoted calcium influx, decreased cell viability, increased apoptosis, and enhanced p38 MAPK phosphorylation in OGD cardiomyocytes (all\n                    <jats:italic>P<\/jats:italic>\n                    \u2009&lt;\u20090.05). These effects were rescued by several calcium\u2010channel blockers (ie, MK\u2010801, La\n                    <jats:sup>3+<\/jats:sup>\n                    , Gap26 peptide, 18\u03b2\u2010glycyrrhetinic acid) but most potently rescued via the NMDAR\u2010specific antagonist MK\u2010801 or removal of extracellular free calcium (all\n                    <jats:italic>P<\/jats:italic>\n                    \u2009&lt;\u20090.05). Knocking\u2010down p38 MAPK activity by small\u2010molecule inhibition or genetic methods significantly increased cell viability and reduced apoptosis (all\n                    <jats:italic>P<\/jats:italic>\n                    \u2009&lt;\u20090.05). Enhancing p38 MAPK activity abolished MK\u2010801\u2032s apoptosis\u2010reducing effects in a p38 MAPK\u2010dependent manner. In conclusion, NMDAR\u2010driven calcium influx promotes apoptosis in ischemic human cardiomyocytes, an effect which can be attributed to enhanced p38 MAPK activity.\n                  <\/jats:p>","DOI":"10.1002\/jcb.27702","type":"journal-article","created":{"date-parts":[[2019,1,7]],"date-time":"2019-01-07T06:14:18Z","timestamp":1546841658000},"page":"4872-4882","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":21,"title":["NMDA receptor\u2010driven calcium influx promotes ischemic human cardiomyocyte apoptosis through a p38 MAPK\u2010mediated mechanism"],"prefix":"10.1002","volume":"120","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1919-3036","authenticated-orcid":false,"given":"Zi\u2010You","family":"Liu","sequence":"first","affiliation":[{"name":"Heart Center, The First Affiliated Hospital of Gannan Medical University Ganzhou Jiangxi China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qin\u2010Wen","family":"Zhong","sequence":"additional","affiliation":[{"name":"Heart Center, The First Affiliated Hospital of Gannan Medical University Ganzhou Jiangxi China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Cheng\u2010Nan","family":"Tian","sequence":"additional","affiliation":[{"name":"Heart Center, The First Affiliated Hospital of Gannan Medical University Ganzhou Jiangxi China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hou Mou","family":"Ma","sequence":"additional","affiliation":[{"name":"Clinical Research Center, The First Affiliated Hospital of Gannan Medical University Ganzhou Jiangxi China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jun\u2010Jian","family":"Yu","sequence":"additional","affiliation":[{"name":"Heart Center, The First Affiliated Hospital of Gannan Medical University Ganzhou Jiangxi China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shuo","family":"Hu","sequence":"additional","affiliation":[{"name":"Heart Center, The First Affiliated Hospital of Gannan Medical University Ganzhou Jiangxi China"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2019,1,6]]},"reference":[{"key":"e_1_2_8_1_2_1","doi-asserted-by":"publisher","DOI":"10.1177\/1073858411435129"},{"key":"e_1_2_8_1_3_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.neuropharm.2011.03.015"},{"key":"e_1_2_8_1_4_1","first-page":"423","article-title":"The NMDA receptor complex: enhancement of memory in aging and dementia","volume":"2","year":"2013","journal-title":"Basic Appl Memory Res"},{"key":"e_1_2_8_1_5_1","doi-asserted-by":"publisher","DOI":"10.1161\/STROKEAHA.115.009314"},{"key":"e_1_2_8_1_6_1","doi-asserted-by":"publisher","DOI":"10.1038\/srep14781"},{"key":"e_1_2_8_1_7_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.neuron.2014.03.030"},{"key":"e_1_2_8_1_8_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0006-8993(99)01322-0"},{"key":"e_1_2_8_1_9_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0361-9230(98)00012-4"},{"key":"e_1_2_8_1_10_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0361-9230(98)00154-3"},{"key":"e_1_2_8_1_11_1","doi-asserted-by":"publisher","DOI":"10.33549\/physiolres.931053"},{"key":"e_1_2_8_1_12_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.cardiores.2003.09.031"},{"key":"e_1_2_8_1_13_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.ejphar.2016.11.053"},{"key":"e_1_2_8_1_14_1","doi-asserted-by":"publisher","DOI":"10.1111\/bph.12794"},{"key":"e_1_2_8_1_15_1","doi-asserted-by":"publisher","DOI":"10.1007\/s11481-012-9362-3"},{"key":"e_1_2_8_1_16_1","doi-asserted-by":"publisher","DOI":"10.1165\/rcmb.2008-0135OC"},{"key":"e_1_2_8_1_17_1","doi-asserted-by":"publisher","DOI":"10.1096\/fj.03-1038fje"},{"key":"e_1_2_8_1_18_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.yjmcc.2012.07.008"},{"key":"e_1_2_8_1_19_1","doi-asserted-by":"publisher","DOI":"10.1631\/jzus.B1600270"},{"key":"e_1_2_8_1_20_1","doi-asserted-by":"publisher","DOI":"10.1016\/S1054-8807(00)00056-9"},{"key":"e_1_2_8_1_21_1","doi-asserted-by":"publisher","DOI":"10.1007\/s00395-004-0478-3"},{"key":"e_1_2_8_1_22_1","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.4.2161"},{"key":"e_1_2_8_1_23_1","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.22.10.3389-3403.2002"},{"key":"e_1_2_8_1_24_1","doi-asserted-by":"publisher","DOI":"10.1038\/ncomms8388"},{"key":"e_1_2_8_1_25_1","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00022.2007"},{"key":"e_1_2_8_1_26_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(03)01017-1"},{"key":"e_1_2_8_1_27_1","doi-asserted-by":"publisher","DOI":"10.1038\/nn835"},{"key":"e_1_2_8_1_28_1","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.1267-12.2012"},{"issue":"3","key":"e_1_2_8_1_29_1","first-page":"1211","article-title":"Ifenprodil and SL 82.0715 as cerebral anti\u2010ischemic agents. 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