The DOI matches its Crossref record; 3 of the 3 references it cites were found in a registry or an index.
Bax ablation protects against myocardial ischemia-reperfusion injury in transgenic mice
Abstract
The role of the proapototic Bax gene in ischemia-reperfusion (I/R) injury was studied in three groups of mice: homozygotic knockout mice lacking the Bax gene (Bax−/−), heterozygotic mice (Bax+/−), and wild-type mice (Bax+/+). Isolated hearts were subjected to ischemia (30 min, 37°C) and then to 120 min of reperfusion. The left ventricular developed force of Bax-deficient vs. Bax+/+ hearts at stabilization and at 120 min of reperfusion was 1,411 ± 177 vs. 1,161 ± 137 mg and 485 ± 69 vs. 306 ± 68 mg, respectively. Superior cardiac function of Bax−/− hearts after I/R was accompanied by a decrease in creatine kinase release, caspase 3 activity, irreversible ischemic injury, and the number of terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling-positive cardiomyocytes. Electron microscopic evaluation revealed reduced damage to mitochondria and the nuclear chromatin structure in Bax-deficient mice. In the Bax+/− hearts, the damage markers were moderate. The superior tolerance of Bax knockout hearts to I/R injury recommends this gene as a potential target for therapeutic intervention in patients with severe and intractable myocardial ischemia.
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Cites
Molecular characterization of mitochondrial apoptosis-inducing factor
Susin, S. A., Lorenzo, H. K., Zamzami, N., Marzo, I., Snow, B. E., Brothers, G. M., Mangion, J., Jacotot, E., Costantini, P., Loeffler, M., et al. (1999) · Nature · doi:10.1038/17135 · Cited by 4,060
Apoptosis in the Failing Human Heart
Olivetti, G., Abbi, R., Quaini, F., Kajstura, J., Cheng, W., Nitahara, J. A., Quaini, E., Di Loreto, C., Beltrami, C. A., Krajewski, S., et al. (1997) · New England Journal of Medicine · doi:10.1056/nejm199704173361603 · Cited by 1,673
Bossy‐Wetzel, E., Newmeyer, D. D., & Green, D. R. (1998) · The EMBO Journal · doi:10.1093/emboj/17.1.37 · Cited by 1,225
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Elmore, S. (2007) · Toxicologic Pathology · doi:10.1080/01926230701320337 · Cited by 13,853
Fundamental Mechanisms of Regulated Cell Death and Implications for Heart Disease
Del Re, D. P., Amgalan, D., Linkermann, A., Liu, Q., & Kitsis, R. N. (2019) · Physiological Reviews · doi:10.1152/physrev.00022.2018 · Cited by 961
Cell Death in the Pathogenesis of Heart Disease: Mechanisms and Significance
Whelan, R. S., Kaplinskiy, V., & Kitsis, R. N. (2010) · Annual Review of Physiology · doi:10.1146/annurev.physiol.010908.163111 · Cited by 759
Molecular machinery and interplay of apoptosis and autophagy in coronary heart disease
Dong, Y., Chen, H., Gao, J., Liu, Y., Li, J., & Wang, J. (2019) · Journal of Molecular and Cellular Cardiology · doi:10.1016/j.yjmcc.2019.09.001 · Cited by 438
Autophagy in Atherosclerosis: A Cell Survival and Death Phenomenon With Therapeutic Potential
Martinet, W., & De Meyer, G. R. Y. (2009) · Circulation Research · doi:10.1161/circresaha.108.188318 · Cited by 381
Metadata
- Authors
- Hochhauser, E., Kivity, S., Offen, D., Maulik, N., Otani, H., Barhum, Y., Pannet, H., Shneyvays, V., Shainberg, A., Goldshtaub, V., Tobar, A., & Vidne, B. A.
- Venue
- American Journal of Physiology-Heart and Circulatory Physiology
- Publisher
- American Physiological Society
- Published
- 2003-06-01
- Volume
- 284
- Issue
- 6
- Pages
- H2351-H2359
- ISSN
- 0363-6135 (ISSN-L)
- 1522-1539
- OpenAlex
- W2069302426
- Cited by
- 224
- References
- 3
- FWCI
- 5.82
- Type
- journal article
- Language
- en
- Open access
- closed
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- Hochhauser, E., Kivity, S., Offen, D., Maulik, N., Otani, H., Barhum, Y., Pannet, H., Shneyvays, V., Shainberg, A., Goldshtaub, V., Tobar, A., & Vidne, B. A. (2003). Bax ablation protects against myocardial ischemia-reperfusion injury in transgenic mice. American Journal of Physiology-Heart and Circulatory Physiology. https://doi.org/10.1152/ajpheart.00783.2002
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