The DOI matches its Crossref record; 4 of the 4 references it cites were found in a registry or an index.
A novel protective effect of erythropoietin in the infarcted heart
Open accessAbstract
Erythropoietin (EPO) has been shown to protect neurons from ischemic stroke, but can also increase thrombotic events and mortality rates in patients with ischemic heart disease. We reasoned that benefits of EPO might be offset by increases in hematocrit and evaluated the direct effects of EPO in the ischemic heart. We show that preconditioning with EPO protects H9c2 myoblasts in vitro and cardiomyocytes in vivo against ischemic injury. EPO treatment leads to significantly improved cardiac function following myocardial infarction. This protection is associated with mitigation of myocyte apoptosis, translating into more viable myocardium and less ventricular dysfunction. EPO-mediated myocyte survival appears to involve Akt activation. Importantly, cardioprotective effects of EPO were seen without an increase in hematocrit (eliminating oxygen delivery as an etiologic factor in myocyte survival and function), demonstrating that EPO can directly protect the ischemic and infarcted heart.
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A Multicenter, Randomized, Controlled Clinical Trial of Transfusion Requirements in Critical Care
Hébert, P. C., Wells, G., Blajchman, M. A., Marshall, J., Martin, C., Pagliarello, G., Tweeddale, M., Schweitzer, I., & Yetisir, E. (1999) · New England Journal of Medicine · doi:10.1056/nejm199902113400601 · Cited by 5,187
Besarab, A., Bolton, W. K., Browne, J. K., Egrie, J. C., Nissenson, A. R., Okamoto, D. M., Schwab, S. J., & Goodkin, D. A. (1998) · New England Journal of Medicine · doi:10.1056/nejm199808273390903 · Cited by 1,930 · cited 2×
“Finally, increases in hematocrit have been linked to excess mortality rates in patients with ischemic heart disease (11, 12).”
BackgroundMitochondrial reactive oxygen species trigger hypoxia-induced transcription
Chandel, N. S., Maltepe, E., Goldwasser, E., Mathieu, C. E., Simon, M. C., & Schumacker, P. T. (1998) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.95.20.11715 · Cited by 1,926
Vanden Hoek, T. L., Becker, L. B., Shao, Z., Li, C., & Schumacker, P. T. (1998) · Journal of Biological Chemistry · doi:10.1074/jbc.273.29.18092 · Cited by 721
Cited by
Ischemia and reperfusion—from mechanism to translation
Eltzschig, H. K., & Eckle, T. (2011) · Nature Medicine · doi:10.1038/nm.2507 · Cited by 3,382
Hydroxylation of HIF-1: Oxygen Sensing at the Molecular Level
Semenza, G. L. (2004) · Physiology · doi:10.1152/physiol.00001.2004 · Cited by 905
Kempf, T., Eden, M., Strelau, J., Naguib, M., Willenbockel, C., Tongers, J., Heineke, J., Kotlarz, D., Xu, J., Molkentin, J. D., et al. (2006) · Circulation Research · doi:10.1161/01.res.0000202805.73038.48 · Cited by 651
Kell, D. B. (2009) · BMC Medical Genomics · doi:10.1186/1755-8794-2-2 · Cited by 554
Chong, Z. Z., Li, F., & Maiese, K. (2005) · Progress in Neurobiology · doi:10.1016/j.pneurobio.2005.02.004 · Cited by 536
Metadata
- Authors
- Parsa, C. J., Matsumoto, A., Kim, J., Riel, R. U., Pascal, L. S., Walton, G. B., Thompson, R. B., Petrofski, J. A., Annex, B. H., Stamler, J. S., & Koch, W. J.
- Venue
- Journal of Clinical Investigation
- Published
- 2003-10-01
- Volume
- 112
- Issue
- 7
- Pages
- 999-1007
- ISSN
- 0021-9738 (ISSN-L)
- OpenAlex
- W2108712459
- Cited by
- 548
- References
- 4
- FWCI
- 22.39
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Parsa, C. J., Matsumoto, A., Kim, J., Riel, R. U., Pascal, L. S., Walton, G. B., Thompson, R. B., Petrofski, J. A., Annex, B. H., Stamler, J. S., & Koch, W. J. (2003). A novel protective effect of erythropoietin in the infarcted heart. Journal of Clinical Investigation. https://doi.org/10.1172/jci18200
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
