{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,8]],"date-time":"2026-03-08T10:23:35Z","timestamp":1772965415558,"version":"3.50.1"},"reference-count":91,"publisher":"Canadian Science Publishing","issue":"8","license":[{"start":{"date-parts":[[2019,8,1]],"date-time":"2019-08-01T00:00:00Z","timestamp":1564617600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/www.nrcresearchpress.com\/page\/about\/CorporateTextAndDataMining"}],"content-domain":{"domain":["cdnsciencepub.com"],"crossmark-restriction":false},"short-container-title":["Can. J. Physiol. Pharmacol."],"published-print":{"date-parts":[[2019,8]]},"abstract":"<jats:p> Myocardial infarction (MI) in mice results in cardiac rupture at 4\u20137 days after MI, whereas cardiac fibrosis and dysfunction occur later. N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) has anti-inflammatory, anti-fibrotic, and pro-angiogenic properties. We hypothesized that Ac-SDKP reduces cardiac rupture and adverse cardiac remodeling, and improves function by promoting angiogenesis and inhibiting detrimental reactive fibrosis and inflammation after MI. C57BL\/6J mice were subjected to MI and treated with Ac-SDKP (1.6 mg\/kg per day) for 1 or 5 weeks. We analyzed (1) intercellular adhesion molecule-1 (ICAM-1) expression; (2) inflammatory cell infiltration and angiogenesis; (3) gelatinolytic activity; (4) incidence of cardiac rupture; (5) p53, the endoplasmic reticulum stress marker CCAAT\/enhancer binding protein homology protein (CHOP), and cardiomyocyte apoptosis; (6) sarcoplasmic reticulum Ca<jats:sup>2+<\/jats:sup> ATPase (SERCA2) expression; (7) interstitial collagen fraction and capillary density; and (8) cardiac remodeling and function. Acutely, Ac-SDKP reduced cardiac rupture, decreased ICAM-1 expression and the number of infiltrating macrophages, decreased gelatinolytic activity, p53 expression, and myocyte apoptosis, but increased capillary density in the infarction border. Chronically, Ac-SDKP improved cardiac structures and function, reduced CHOP expression and interstitial collagen fraction, and preserved myocardium SERCA2 expression. Thus, Ac-SDKP decreased cardiac rupture, ameliorated adverse cardiac remodeling, and improved cardiac function after MI, likely through preserved SERCA2 expression and inhibition of endoplasmic reticulum stress. <\/jats:p>","DOI":"10.1139\/cjpp-2019-0047","type":"journal-article","created":{"date-parts":[[2019,4,18]],"date-time":"2019-04-18T21:39:26Z","timestamp":1555623566000},"page":"753-765","update-policy":"https:\/\/doi.org\/10.1139\/csp-crossmark-policy","source":"Crossref","is-referenced-by-count":6,"title":["<i>N<\/i>-acetyl-seryl-aspartyl-lysyl-proline treatment protects heart against excessive myocardial injury and heart failure in mice"],"prefix":"10.1139","volume":"97","author":[{"given":"Hongmei","family":"Peng","sequence":"first","affiliation":[{"name":"Hypertension and Vascular Research Division, Department of Internal Medicine, Detroit, MI 48202, USA."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jiang","family":"Xu","sequence":"additional","affiliation":[{"name":"Hypertension and Vascular Research Division, Department of Internal Medicine, Detroit, MI 48202, USA."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Xiao-Ping","family":"Yang","sequence":"additional","affiliation":[{"name":"Hypertension and Vascular Research Division, Department of Internal Medicine, Detroit, MI 48202, USA."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kamal M.","family":"Kassem","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, University of Cincinnati Medical Center, Cincinnati, OH 45219, USA."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Imane A.","family":"Rhaleb","sequence":"additional","affiliation":[{"name":"Hypertension and Vascular Research Division, Department of Internal Medicine, Detroit, MI 48202, USA."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ed","family":"Peterson","sequence":"additional","affiliation":[{"name":"Department of Public Health Sciences, Henry Ford Hospital, Detroit, MI 48202, USA."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Nour-Eddine","family":"Rhaleb","sequence":"additional","affiliation":[{"name":"Hypertension and Vascular Research Division, Department of Internal Medicine, Detroit, MI 48202, USA."},{"name":"Department of Physiology, Wayne State University, Detroit, MI 48201, USA."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"155","reference":[{"key":"refg1\/ref1","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.0000338496.95579.56"},{"key":"refg2\/ref2","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118484"},{"key":"refg3\/ref3","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M707539200"},{"issue":"4","key":"refg4\/ref4","doi-asserted-by":"crossref","first-page":"836","DOI":"10.1681\/ASN.V134836","volume":"13","author":"Biner H.L.","year":"2002","journal-title":"J. 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