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• W2082002012 abstract "Cardiac troponin (cTn) is an intracellular protein that is expressed by normal myocardial cells. Myocardial cell injuries that are caused by severe myocardial ischemia can lead to the persistent release of cTn, which results in a sustained elevation in the peripheral circulation that can last approximately 5–7 days for cTn I and 7–14 days for cTn T [ [1] Alpert J.S. Thygesen K. White H.D. Jaffe A.S. Implications of the universal definition of myocardial infarction. Nat Clin Pract Cardiovasc Med. 2008; 5: 678-679 Crossref PubMed Scopus (13) Google Scholar ]. During this process, many types of cells, including myocardial cells, are exposed to high concentrations of cTn in the extracellular fluid. However, it is unknown whether a sustained high concentration of cTn has direct biological effects on adjacent myocardial cells during serious ischemic injury. To address this issue, the present study established an in vitro hypoxia/reoxygenation model using myocardial cells that were isolated from neonatal rats to determine whether exogenous cTn I affects the myocardial cell injuries that are incurred during the process of hypoxia/reoxygenation." @default.
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• W2082002012 date "2012-06-01" @default.
• W2082002012 modified "2023-10-03" @default.
• W2082002012 title "Cardiac troponin I reduces hypoxia/reoxygenation-induced myocardial cell injury in vitro" @default.
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• W2082002012 doi "https://doi.org/10.1016/j.ijcard.2012.04.055" @default.
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