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• W2005376600 abstract "High mobility group box 1 protein (HMGB1), a non-chromosomal nuclear protein that regulates gene transcription and maintains the nucleosome structure, could be negatively released by necrotic cell, apoptotic cell or positively activated innate immune cells (such as macrophages and monocytes) [ 1 Scaffidi P. Misteli T. Bianchi M.E. Release of chromatin protein HMGB1 by necrotic cells triggers inflammation. Nature. 2002; 418: 191-195 Crossref PubMed Scopus (3303) Google Scholar , 2 Bell C.W. Jiang W. Reich C.F. et al. The extracellular release of HMGB1 during apoptotic cell death. Am J Physiol Cell Physiol. 2006; 291: C1318-C1325 Crossref PubMed Scopus (419) Google Scholar ]. HMGB1 has been identified as a novel pro-inflammatory cytokine in several cardiovascular diseases [ 3 Andrassy M. Volz H.C. Igwe J.C. et al. High-mobility group box-1 in ischemia-reperfusion injury of the heart. Circulation. 2008; 117: 3216-3226 Crossref PubMed Scopus (520) Google Scholar , 4 Hu X. Jiang H. Bai Q. et al. Increased serum HMGB1 is related to the severity of coronary artery stenosis. Clin Chim Acta. 2009; 406: 139-142 Crossref PubMed Scopus (59) Google Scholar , 5 Andrassy M. Volz H.C. Riedle N. et al. HMGB1 as a predictor of infarct transmurality and functional recovery in patients with myocardial infarction. J Intern Med. 2011; 270: 245-253 Crossref PubMed Scopus (55) Google Scholar , 6 Zhao D. Wang Y. Xu Y. Decreased serum endogenous secretory receptor for advanced glycation endproducts and increased cleaved receptor for advanced glycation endproducts levels in patients with atrial fibrillation. Int J Cardiol. 2012; 158: 471-472 Abstract Full Text Full Text PDF PubMed Scopus (15) Google Scholar ]. Recently HMGB1 has been found to function as an early pro-inflammatory mediator during myocardial ischemia and reperfusion (I/R) as well as classical early pro-inflammatory cytokines such as tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and could promote the release of TNF-α and IL-6, whereas HMGB1 A box peptide (a specific HMGB1 antagonist) could protect against myocardial I/R injury and inhibit the release of TNF-α and IL-6 [ [3] Andrassy M. Volz H.C. Igwe J.C. et al. High-mobility group box-1 in ischemia-reperfusion injury of the heart. Circulation. 2008; 117: 3216-3226 Crossref PubMed Scopus (520) Google Scholar ]. While inflammatory response is considered to be a critical factor of myocardial I/R injury [ 7 Frangoginis N.G. Smith C.W. Entman M.L. The inflammatory response in myocardial infarction. Cardiovasc Res. 2002; 53: 31-47 Crossref PubMed Scopus (1714) Google Scholar , 8 Hu X. Fu W. Jiang H. HMGB1: a potential therapeutic target for myocardial ischemia and reperfusion injury. Int J Cardiol. 2012; 155: 489-489 Abstract Full Text Full Text PDF Scopus (26) Google Scholar ]. These results suggested that HMGB1 plays an important role in myocardial I/R injury." @default.
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• W2005376600 date "2013-10-01" @default.
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• W2005376600 title "Short-time pretreatment of rosuvastatin attenuates myocardial ischemia and reperfusion injury by inhibiting high mobility group box 1 protein expression" @default.
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• W2005376600 doi "https://doi.org/10.1016/j.ijcard.2013.07.074" @default.
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