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Acute cellular actions of thyroid hormone and myocardial function
The Annals of Thoracic Surgery
|July 1, 1993
Summary
Thyroid hormone exerts acute, extranuclear effects on the heart, influencing calcium (Ca2+) handling by affecting Ca(2+)-adenosine triphosphatases (ATPases). These actions may improve heart function and offer cardioprotection.
Area of Science:
- Cardiology
- Endocrinology
- Molecular Biology
Background:
- Thyroid hormone actions are typically nuclear-mediated.
- Emerging evidence suggests extranuclear mechanisms for thyroid hormone's effects.
- These extranuclear actions are particularly relevant in cardiac tissue.
Purpose of the Study:
- To review the acute, extranuclear mechanisms of thyroid hormone action on the heart.
- To explore the impact of these mechanisms on cardiac calcium (Ca2+) handling.
- To discuss the potential cardioprotective roles of these extranuclear effects.
Main Methods:
- Review of existing literature on thyroid hormone's extranuclear effects.
- Analysis of studies investigating thyroid hormone's influence on myocardial Ca(2+)-adenosine triphosphatases (ATPases).
- Examination of effects on sarcolemmal and sarcoplasmic reticulum Ca(2+)-ATPase activity.
Main Results:
- Thyroid hormone acutely affects myocardial sarcolemmal and sarcoplasmic reticulum Ca(2+)-adenosine triphosphatases (ATPases) via extranuclear pathways.
- These actions can reduce cytoplasmic [Ca2+], enhancing myocardial relaxation and diastolic function.
- Potential for cardioprotection during ischemia-reperfusion injury by modulating sarcoplasmic [Ca2+].
Conclusions:
- Thyroid hormone has significant acute, extranuclear effects on cardiac calcium (Ca2+) regulation.
- These extranuclear mechanisms contribute to improved myocardial relaxation and may be cardioprotective.
- Further research into these extranuclear actions could reveal novel therapeutic targets for heart failure and ischemia.