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Author Spotlight: In Vivo Assessment of Thyroid Hormone Disruption Using the THAI Mouse Model
Published on: October 6, 2023
Thyroid hormone action in postnatal heart development
Ming Li1, Siiri E Iismaa2, Nawazish Naqvi3
1Victor Chang Cardiac Research Institute, Darlinghurst, NSW 2010, Australia.
Insights
Thyroid hormone stimulates cardiomyocyte proliferation for postnatal cardiac development. Altered thyroid hormone metabolism in disease impairs heart function, but T3 therapy may improve contractility.
Area of Science:
- Cardiology
- Endocrinology
- Developmental Biology
Background:
- Thyroid hormone is essential for fetal and postnatal cardiac growth.
- Recent findings highlight its role in stimulating cardiomyocyte proliferation during preadolescence.
- Thyroid hormone metabolism is disrupted in chronic diseases like heart failure, leading to low T3 syndrome.
Purpose of the Study:
- To review the role of thyroid hormone in postnatal cardiac development.
- To explore the impact of altered thyroid hormone metabolism on cardiovascular function.
- To consider therapeutic strategies involving thyroid hormone analogs for cardiac conditions.
Main Methods:
- Review of existing literature on thyroid hormone and cardiac development.
- Analysis of studies on cardiomyocyte proliferation in response to thyroid hormone.
- Examination of clinical data regarding thyroid hormone levels in heart disease.
Main Results:
- Thyroid hormone drives a significant burst of cardiomyocyte proliferation in the murine heart during preadolescence.
- Low T3 syndrome, associated with chronic diseases, impairs cardiovascular function and prognosis.
- Thyroid hormone analogs show potential in improving cardiac contractility, though mechanisms are unclear.
Conclusions:
- Thyroid hormone plays a crucial role in postnatal cardiac development through cardiomyocyte proliferation.
- Dysregulation of thyroid hormone metabolism in disease negatively impacts cardiac function.
- Further research into T3's mitogenic potential for cardiomyocytes is warranted for therapeutic development.
Abstract:
Thyroid hormone is a critical regulator of cardiac growth and development, both in fetal life and postnatally. Here we review the role of thyroid hormone in postnatal cardiac development, given recent insights into its role in stimulating a burst of cardiomyocyte proliferation in the murine heart in preadolescence; a response required to meet the massive increase in circulatory demand predicated by an almost quadrupling of body weight during a period of about 21 days from birth to adolescence. Importantly, thyroid hormone metabolism is altered by chronic diseases, such as heart failure and ischemic heart disease, as well as in very sick children requiring surgery for congenital heart diseases, which results in low T3 syndrome that impairs cardiovascular function and is associated with a poor prognosis. Therapy with T3 or thyroid hormone analogs has been shown to improve cardiac contractility; however, the mechanism is as yet unknown. Given the postnatal cardiomyocyte mitogenic potential of T3, its ability to enhance cardiac function by promoting cardiomyocyte proliferation warrants further consideration.
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