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Acute cellular actions of thyroid hormone and myocardial function
Abstract:
The mechanisms of actions of thyroid hormone in various tissues are largely viewed as cell nucleus-mediated. However, several actions of this hormone are definitively extranuclear, and these include effects on the activities of Ca(2+)-adenosine triphosphatases (ATPases) of myocardial sarcolemma and, apparently, sarcoplasmic reticulum in animal models. Both effects would serve to reduce cytoplasmic (sarcoplasmic) [Ca2+]. Sarcoplasmic reticulum uptake of Ca2+ from sarcoplasm is mediated by Ca(2+)-ATPase and is deficient in end-stage heart failure; thyroid hormone can enhance sarcoplasmic reticulum Ca(2+)-ATPase activity acutely via an extranuclear mechanism or indirectly via the myosin-associated Ca(2+)-ATPase gene. Such actions would serve to improve myocardial relaxation, thus improvement in diastolic dysfunction, and may be cardioprotective if excessive levels of sarcoplasmic [Ca2+] develop during reperfusion of previously ischemic tissue. Action of thyroid hormone on sarcolemmal Ca(2+)-ATPase activity will enhance Ca2+ efflux, and a recently described effect of the hormone on myocardial Na+ inactivation current may serve to increase or reduce sarcoplasmic [Ca2+], depending upon the vector of Na+/Ca2+ exchange. This article reviews acute effects of thyroid hormone on the heart that are extranuclear in mechanism.
Insights
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.