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Mechano-chemo-transduction in cardiac myocytes
Ye Chen-Izu1,2,3, Leighton T Izu1
1Department of Pharmacology, University of California, Davis, CA, 95616, USA.
The Journal of Physiology
|January 19, 2017
Summary
The heart adjusts contraction force via intrinsic mechanisms like the Frank-Starling law and Anrep effect. Cellular sensors modulate reactive oxygen and nitric oxide signaling, impacting calcium handling and cardiac output regulation.
Area of Science:
- Cardiovascular Physiology
- Cellular Mechanotransduction
Background:
- The heart autoregulates contraction force to maintain cardiac output under varying preload and afterload.
- Cellular and molecular mechanisms underlying the Frank-Starling law and Anrep effect remain debated.
- Understanding how cardiac myocytes sense and respond to mechanical load is crucial.
Purpose of the Study:
- To review and compare recent studies on how cardiac myocytes sense mechanical load.
- To elucidate the cellular and molecular pathways involved in mechanical signal transduction.
- To explore the role of these pathways in regulating calcium handling and cardiac function.
Main Methods:
- Comparative analysis of recent experimental studies.
- Focus on the 'dimensionality' of the mechanical environment in experiments.
- Examination of cellular and surface mechanosensor roles.
Main Results:
- Mechanosensors within myocytes appear to modulate reactive oxygen species (ROS) signaling.
- Cell surface mechanosensors seem to modulate nitric oxide (NO) signaling.
- Both ROS and NO signaling pathways influence intracellular calcium (Ca2+) handling.
Conclusions:
- Cellular mechanics are intimately linked to ROS and NO signaling, affecting Ca2+ handling.
- This provides deeper insight into the Frank-Starling law and Anrep effect.
- Understanding these links may unify our view on mechanobiology-related arrhythmias.
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