{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,8]],"date-time":"2026-04-08T11:21:25Z","timestamp":1775647285265,"version":"3.50.1"},"reference-count":30,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2020,3,16]],"date-time":"2020-03-16T00:00:00Z","timestamp":1584316800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["febs.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["FEBS Open Bio"],"published-print":{"date-parts":[[2020,4]]},"abstract":"<jats:p>\n                    Myocardial ischemia\/reperfusion (I\/R) injury is a major complication of reperfusion therapy in myocardial infarction. Ischemic myocardium produces a variety of peptides. We recently identified PDRPS7 as a novel peptide in cardiomyocytes that can be induced by hypoxia. However, the role of PDRPS7 is unknown. Here, we investigated the effects of PDRPS7 on hypoxia\/reoxygenation (H\/R)\u2010induced injury in rat cardiomyoblast H9c2 cells and NRCMs. We found that PDRPS7 improved cell survival and attenuated lactate dehydrogenase leakage following H\/R in H9c2 cells and NRCMs. PDRPS7 also alleviated H\/R\u2010induced pulsation reduction in NRCMs. Moreover, H\/R\u2010induced cell apoptosis was decreased in the presence of PDRPS7. H\/R\u2010induced reactive oxygen species generation was reduced by PDRPS7; in addition, PDRPS7 did not impact H\n                    <jats:sub>2<\/jats:sub>\n                    O\n                    <jats:sub>2<\/jats:sub>\n                    \u2010induced cell injury. Signaling analysis demonstrated that H\/R increased the phosphorylation levels of JNKs, ERKs, and p38 mitogen\u2010activated protein kinases. However, PDRPS7 only attenuated H\/R\u2010induced JNK phosphorylation, but not phosphorylation of ERKs and p38. PDRPS7 protected cardiomyocytes from apoptosis by inhibiting JNK phosphorylation and c\u2010Jun phosphorylation pathways, markedly upregulating anti\u2010apoptotic Bcl\u20102 expression and inhibiting that of pro\u2010apoptotic Bax and cleaved caspase\u20103. Importantly, pharmacological activation of JNKs diminished the protective effect of PDRPS7 in terms of cell survival against H\/R stimulation. In summary, our study identified PDRPS7 as a novel cardioprotective peptide against H\/R challenge and this action was mediated, at least in part, through inactivation of JNKs.\n                  <\/jats:p>","DOI":"10.1002\/2211-5463.12822","type":"journal-article","created":{"date-parts":[[2020,2,28]],"date-time":"2020-02-28T09:40:57Z","timestamp":1582882857000},"page":"593-606","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":5,"title":["PDRPS7 protects cardiac cells from hypoxia\/reoxygenation injury through inactivation of JNKs"],"prefix":"10.1002","volume":"10","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-5424-3003","authenticated-orcid":false,"given":"Yulian","family":"Duan","sequence":"first","affiliation":[{"name":"College of Life Sciences Nanjing Normal University 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