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Cited by 301

The DOI matches its Crossref record; 6 of the 6 references it cites were found in a registry or an index.

Inhibition of ischemic cardiomyocyte apoptosis through targeted ablation of Bnip3 restrains postinfarction remodeling in mice

Open access
Diwan, Abhinav, Krenz, Maike, Syed, Faisal M., Wansapura, Janaka, Ren, Xiaoping, Koesters, Andrew G., Li, Hairong, Kirshenbaum, Lorrie A., Hahn, Harvey S., Robbins, Jeffrey, Jones, W. Keith, Dorn, Gerald W.·2007·Journal of Clinical Investigation

Abstract

Following myocardial infarction, nonischemic myocyte death results in infarct expansion, myocardial loss, and ventricular dysfunction. Here, we demonstrate that a specific proapoptotic gene, Bnip3, minimizes ventricular remodeling in the mouse, despite having no effect on early or late infarct size. We evaluated the effects of ablating Bnip3 on cardiomyocyte death, infarct size, and ventricular remodeling after surgical ischemia/reperfusion (IR) injury in mice. Immediately following IR, no significant differences were observed between Bnip3(-/-) and WT mice. However, at 2 days after IR, apoptosis was diminished in Bnip3(-/-) periinfarct and remote myocardium, and at 3 weeks after IR, Bnip3(-/-) mice exhibited preserved LV systolic performance, diminished LV dilation, and decreased ventricular sphericalization. These results suggest myocardial salvage by inhibition of apoptosis. Forced cardiac expression of Bnip3 increased cardiomyocyte apoptosis in unstressed mice, causing progressive LV dilation and diminished systolic function. Conditional Bnip3 overexpression prior to coronary ligation increased apoptosis and infarct size. These studies identify postischemic apoptosis by myocardial Bnip3 as a major determinant of ventricular remodeling in the infarcted heart, suggesting that Bnip3 may be an attractive therapeutic target.

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Metadata

Authors
Diwan, A., Krenz, M., Syed, F. M., Wansapura, J., Ren, X., Koesters, A. G., Li, H., Kirshenbaum, L. A., Hahn, H. S., Robbins, J., Jones, W. K., & Dorn, G. W.
Venue
Journal of Clinical Investigation
Published
2007-10-01
Volume
117
Issue
10
Pages
2825-2833
ISSN
0021-9738 (ISSN-L)
OpenAlex
W2020396176
Cited by
301
References
6
FWCI
10.57
Type
journal article
Language
en
Open access
bronze

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CoChat. (2026). Citation check: Inhibition of ischemic cardiomyocyte apoptosis through targeted ablation of Bnip3 restrains postinfarction remodeling in mice. https://app.cochat.ai/papers/10.1172/jci32490
The paper
Diwan, A., Krenz, M., Syed, F. M., Wansapura, J., Ren, X., Koesters, A. G., Li, H., Kirshenbaum, L. A., Hahn, H. S., Robbins, J., Jones, W. K., & Dorn, G. W. (2007). Inhibition of ischemic cardiomyocyte apoptosis through targeted ablation of Bnip3 restrains postinfarction remodeling in mice. Journal of Clinical Investigation. https://doi.org/10.1172/jci32490

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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.