期刊
HEART FAILURE REVIEWS
卷 16, 期 1, 页码 79-96出版社
SPRINGER
DOI: 10.1007/s10741-010-9185-3
关键词
Cardiac hypertrophy; Cardiac remodeling; Heart failure; Myocardial infarction; Myocardial ischemia; Thyroid hormone; Thyroid hormone signaling
资金
- S. Niarchos Foundation
Chronic ischemia or pressure overload decreases thyroid hormone (TH) signaling and activates the fetal gene program in the heart. While these features are of physiologic importance in the developing heart, their respective roles in the postnatal heart are debated. Administration of TH can prevent the changes of the fetal gene program and rebuild the heart after an index event such as ischemia. TH affects cardiac remodeling by limiting reperfusion injury, and, at later states, by inducing distinct changes in cardiac chamber geometry in a time-dependent manner. Furthermore, administration of TH can convert pathologic to physiologic hypertrophy. These effects are the result of favorable cellular remodeling. While preliminary clinical studies provide encouraging results, the potential and efficacy of TH in the treatment of heart disease still await evaluation in large clinical trials.
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