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Clock genes in the heart: characterization and attenuation with hypertrophy
M E Young1, P Razeghi, H Taegtmeyer
1Department of Internal Medicine, Division of Cardiology, University of Texas-Houston Medical School, Houston, TX 77030, USA.
Circulation Research
|June 9, 2001
Summary
The mammalian heart has internal circadian clocks, but pressure overload-induced heart hypertrophy disrupts these biological rhythms. This disruption impairs the heart's ability to anticipate and adapt to daily physiological changes.
Area of Science:
- Cardiology
- Chronobiology
- Molecular Biology
Background:
- Mammalian organs possess internal biological clocks that anticipate environmental stimuli.
- Circadian rhythms are crucial for synchronizing cellular responses with external cues.
- The presence and function of cardiac clock mechanisms in response to stress are not well understood.
Purpose of the Study:
- To investigate the existence of internal clocks in the mammalian heart.
- To determine if pressure overload-induced cardiac hypertrophy affects the cardiac clock mechanism.
Main Methods:
- Examined the expression patterns of known Drosophila clock gene homologues in rat hearts.
- Assessed the induction of clock output genes, specifically PAR transcription factors (dbp, hlf, tef), in normal and hypertrophied hearts.
Main Results:
- All mammalian homologues of Drosophila clock genes exhibit circadian expression patterns in the rat heart.
- The induction of clock output genes (dbp, hlf, tef) is significantly attenuated in pressure-overloaded hypertrophied hearts.
- Cardiac hypertrophy leads to a partial loss of this dynamic regulatory system in the heart.
Conclusions:
- The mammalian heart possesses intrinsic circadian clock mechanisms.
- Pressure overload-induced cardiac hypertrophy impairs the cardiac clock, leading to a diminished ability to anticipate and adapt to daily physiological changes.
- This study reveals a novel regulatory system in the heart that is compromised by hypertrophy.