The DOI matches its Crossref record; 43 of the 43 references it cites were found in a registry or an index.
Histone deacetylase inhibition reduces myocardial ischemia‐reperfusion injury in mice
Open accessAbstract
Limitation of infarct size is a major goal of therapy for acute coronary syndromes, and research has focused on achieving rapid patency of infarct‐related vessels. However, new understandings of epigenetic modifications during ischemia suggest additional targeted approaches that have not been extensively explored. Here, we show that ischemia induces histone deacetylase (HDAC) activity in the heart with deacetylation of histones H3/4 in vitro and in vivo. We show, utilizing a standard murine model of ischemia‐reperfusion, that chemical HDAC inhibitors significantly reduce infarct area, even when delivered 1 h after the ischemic insult. We demonstrate that HDAC inhibitors prevent ischemia‐induced activation of gene programs that include hypoxia inducible factor‐1α, cell death, and vascular permeability in vivo and in vitro , thus providing potential mechanisms to explain reduced vascular leak and myocardial injury. In vitro , siRNA knockdown experiments implicate HDAC4 as a mediator of the effects in ischemic cardiac myocytes. These results demonstrate that HDAC inhibitors alter the response to ischemic injury in the heart and reduce infarct size, suggesting novel therapeutic approaches for acute coronary syndromes.—Granger, A., Abdullah, I., Huebner, F., Stout, A., Wang, T., Huebner, T., Epstein, J. A., Gruber, P. J. Histone deacetylase inhibition reduces myocardial ischemia‐reperfusion injury in mice. FASEB J. 22, 3549–3560 (2008)
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Citations
Cites
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Histone deacetylase inhibitors and the promise of epigenetic (and more) treatments for cancer
Minucci, S., & Pelicci, P. G. (2006) · Nature Reviews Cancer · doi:10.1038/nrc1779 · Cited by 2,200
Regulation of Mammalian O 2 Homeostasis by Hypoxia-Inducible Factor 1
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“In response to hypoxia, HIF1A accumulates and directly induces the transcriptional activity of a number of genes, including genes that control angiogenesis (such as Vegfa) and energy metabolism [for example, the glucose transporter 1 (GLUT1/Scl2a1), 6-phosphofructo-2-kinase/ fructose-2,6-biphosphatase 3 (PFKFB3/Pfkfb3…”
BackgroundHistone and chromatin cross-talk
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Acetylation: a regulatory modification to rival phosphorylation?
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Class II Histone Deacetylases Act as Signal-Responsive Repressors of Cardiac Hypertrophy
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Pathophysiological consequences of VEGF-induced vascular permeability
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Histone methylation in transcriptional control
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Cited by
Kalogeris, T., Baines, C. P., Krenz, M., & Korthuis, R. J. (2016) · Comprehensive Physiology · doi:10.1002/cphy.c160006 · Cited by 718
Multiple roles of HDAC inhibition in neurodegenerative conditions
Chuang, D.-M., Leng, Y., Marinova, Z., Kim, H.-J., & Chiu, C.-T. (2009) · Trends in Neurosciences · doi:10.1016/j.tins.2009.06.002 · Cited by 676
Epigenetics: a molecular link between environmental factors and type 2 diabetes
Ling, C., & Groop, L. (2009) · Diabetes · doi:10.2337/db09-1003 · Cited by 617
Epigenetic regulation of gene expression in physiological and pathological brain processes
Gräff, J., Kim, D., Dobbin, M. M., & Tsai, L.-H. (2011) · Physiological Reviews · doi:10.1152/physrev.00012.2010 · Cited by 373
Lysine acetyltransferases and lysine deacetylases as targets for cardiovascular disease
Li, P., Ge, J., & Li, H. (2020) · Nature Reviews Cardiology · doi:10.1038/s41569-019-0235-9 · Cited by 269
Metadata
- Authors
- Granger, A., Abdullah, I., Huebner, F., Stout, A., Wang, T., Huebner, T., Epstein, J. A., & Gruber, P. J.
- Venue
- The FASEB Journal
- Publisher
- Wiley
- Published
- 2008-07-07
- Volume
- 22
- Issue
- 10
- Pages
- 3549-3560
- ISSN
- 0892-6638 (ISSN-L)
- 1530-6860
- OpenAlex
- W1992670654
- Cited by
- 273
- References
- 43
- FWCI
- 11.80
- Type
- journal article
- Language
- en
- Open access
- green
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