Key result
Sustained changes in cardiac workload (hypertrophy and atrophy) in rat hearts resulted in downregulation of PDK4, MCD, and UCP-3 transcripts, mediated by diminished PPARalpha expression.
Population
Rat heart models of hypertrophy and atrophy
Design
Preclinical
Authors
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Diminished PPARalpha may drive metabolic transcript shifts in rat cardiac remodeling; leaves open therapeutic targeting in human heart failure.
Hypertrophy and atrophy in rat hearts induce a uniform metabolic switch from fatty acid to glucose oxidation through the downregulation of PPARalpha and its target genes.
Taegtmeyer et al. (2002) studied Cardiac hypertrophy and atrophy. Altered cardiac workload (hypertrophy and atrophy) vs. Normal cardiac workload was evaluated on Transcript levels of PDK4, MCD, and UCP-3. Sustained changes in cardiac workload (hypertrophy and atrophy) in rat hearts resulted in downregulation of PDK4, MCD, and UCP-3 transcripts, mediated by diminished PPARalpha expression.
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