The DOI matches its Crossref record; 41 of the 41 references it cites were found in a registry or an index.
Hypoxic Preconditioning Enhances the Benefit of Cardiac Progenitor Cell Therapy for Treatment of Myocardial Infarction by Inducing CXCR4 Expression
Open accessAbstract
Myocardial infarction rapidly depletes the endogenous cardiac progenitor cell pool, and the inefficient recruitment of exogenously administered progenitor cells limits the effectiveness of cardiac cell therapy. Recent reports indicate that interactions between the CXC chemokine stromal cell–derived factor 1 and its receptor CXC chemokine receptor 4 (CXCR4) critically mediate the ischemia-induced recruitment of bone marrow–derived circulating stem/progenitor cells, but the expression of CXCR4 in cardiac progenitor cells is very low. Here, we studied the influence of hypoxia on CXCR4 expression in cardiac progenitor cells, on the recruitment of intravenously administered cells to ischemic heart tissue, and on the preservation of heart function in a murine myocardial infarction model. We found that hypoxic preconditioning increased CXCR4 expression in CLK (cardiosphere-derived, Lin − c-kit + progenitor) cells and markedly augmented CLK cell migration (in vitro) and recruitment (in vivo) to the ischemic myocardium. Four weeks after surgically induced myocardial infarction, infarct size and heart function were significantly better in mice administered hypoxia-preconditioned CLK cells than in mice treated with cells cultured under normoxic conditions. Furthermore, these effects were largely abolished by the addition of a CXCR4 inhibitor, indicating that the benefits of hypoxic preconditioning are mediated by the stromal cell–derived factor 1/CXCR4 axis, and that therapies targeting this axis may enhance cardiac-progenitor cell–based regenerative therapy.
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Cites
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Cited by
Chen, L., Wang, Y., Pan, Y., Zhang, L., Shen, C., Qin, G., Ashraf, M., Weintraub, N., Ma, G., & Tang, Y. (2013) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2013.01.015 · Cited by 359
Self-citationGenetic Engineering of Mesenchymal Stem Cells and Its Application in Human Disease Therapy
Hodgkinson, C. P., Gomez, J. A., Mirotsou, M., & Dzau, V. J. (2010) · Human Gene Therapy · doi:10.1089/hum.2010.165 · Cited by 150
Genetics of leukocyte telomere length and its role in atherosclerosis
Aviv, A. (2012) · Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis · doi:10.1016/j.mrfmmm.2011.05.001 · Cited by 143
Hypoxia-Induced Secretion of TGF-β1 in Mesenchymal Stem Cell Promotes Breast Cancer Cell Progression
Hung, S.-P., Yang, M.-H., Tseng, K.-F., & Lee, O. K. (2013) · Cell Transplantation · doi:10.3727/096368912x657954 · Cited by 137
Ma, H.-C. (2014) · World Journal of Gastroenterology · doi:10.3748/wjg.v20.i40.14884 · Cited by 75
Metadata
- Authors
- Tang, Y. L., Zhu, W., Cheng, M., Chen, L., Zhang, J., Sun, T., Kishore, R., Phillips, M. I., Losordo, D. W., & Qin, G.
- Venue
- Circulation Research
- Published
- 2009-05-22
- Volume
- 104
- Issue
- 10
- Pages
- 1209-1216
- ISSN
- 0009-7330 (ISSN-L)
- 1524-4571
- OpenAlex
- W2170252071
- Cited by
- 363
- References
- 41
- FWCI
- 14.18
- Type
- journal article
- Language
- en
- Open access
- green
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- CoChat. (2026). Citation check: Hypoxic Preconditioning Enhances the Benefit of Cardiac Progenitor Cell Therapy for Treatment of Myocardial Infarction by Inducing CXCR4 Expression. https://app.cochat.ai/papers/10.1161/circresaha.109.197723
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- Tang, Y. L., Zhu, W., Cheng, M., Chen, L., Zhang, J., Sun, T., Kishore, R., Phillips, M. I., Losordo, D. W., & Qin, G. (2009). Hypoxic Preconditioning Enhances the Benefit of Cardiac Progenitor Cell Therapy for Treatment of Myocardial Infarction by Inducing CXCR4 Expression. Circulation Research. https://doi.org/10.1161/circresaha.109.197723
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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.
