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Maintenance of cardiac energy metabolism by histone deacetylase 3 in mice
Rusty L Montgomery1, Matthew J Potthoff, Michael Haberland
1Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
The Journal of Clinical Investigation
|October 3, 2008
Summary
Histone deacetylase 3 (HDAC3) deletion in the heart causes cardiac hypertrophy and metabolic dysfunction. This reveals HDAC3
Area of Science:
- Cardiovascular Biology
- Molecular Biology
- Metabolic Regulation
Background:
- Histone deacetylase (HDAC) inhibitors have therapeutic potential for various diseases.
- The specific roles of individual HDAC isoforms in vivo remain largely unknown.
- Understanding HDAC functions is crucial for targeted therapies.
Purpose of the Study:
- To investigate the role of Histone deacetylase 3 (HDAC3) in cardiac function and metabolism.
- To determine the physiological and pathological functions of HDAC3 in the heart.
Main Methods:
- Generation of mice with a cardiac-specific Hdac3 null allele.
- Analysis of cardiac phenotype, gene expression, and metabolic parameters in Hdac3-deficient mice.
- Comparison with other Hdac gene mutations.
Main Results:
- Cardiac-specific deletion of Hdac3 led to massive cardiac hypertrophy and myocardial lipid accumulation.
- Upregulation of genes involved in fatty acid metabolism and oxidative phosphorylation was observed.
- Abnormalities were linked to excessive activity of the nuclear receptor PPARalpha.
- The phenotype differed from mutations in other Hdac genes.
Conclusions:
- HDAC3 plays a unique and critical role in maintaining cardiac function.
- HDAC3 is essential for the regulation of myocardial energy metabolism.
- Targeting HDAC3 may offer novel therapeutic strategies for cardiac disorders.
