Wassner Ari J, Jugo Rebecca H, Dorfman David M, Padera Robert F, Maynard Michelle A, Zavacki Ann M, Jay Patrick Y, Huang Stephen A
1 Thyroid Program, Division of Endocrinology, Boston Children's Hospital , Boston, Massachusetts.
2 Department of Pathology, Brigham and Women's Hospital , Boston, Massachusetts.
Thyroid. 2017 May;27(5):732-737. doi: 10.1089/thy.2016.0570. Epub 2017 Apr 5.
The thyroid hormone-inactivating enzyme type 3 deiodinase (D3) is induced during hypertrophic and ischemic cardiomyopathy, leading to a state of local cardiac hypothyroidism. Whether D3 induction occurs in dilated cardiomyopathy is unknown.
This study characterized changes in cardiac D3 and thyroid hormone signaling in a transgenic model of progressive dilated cardiomyopathy (TG9 mice).
Cardiac D3 was dramatically induced 15-fold during the progression of dilated cardiomyopathy in TG9 mice. This D3 induction localized to cardiomyocytes and was associated with a decrease in myocardial thyroid hormone signaling.
Cardiac D3 is induced in a mouse model of dilated cardiomyopathy, indicating that D3 induction may be a general response to diverse forms of cardiomyopathy.
3型脱碘酶(D3)是一种甲状腺激素失活酶,在肥厚性心肌病和缺血性心肌病期间被诱导产生,导致局部心脏甲状腺功能减退状态。D3在扩张型心肌病中是否被诱导尚不清楚。
本研究对进行性扩张型心肌病转基因模型(TG9小鼠)中心脏D3和甲状腺激素信号的变化进行了表征。
在TG9小鼠扩张型心肌病进展过程中,心脏D3显著诱导增加了15倍。这种D3诱导定位于心肌细胞,并与心肌甲状腺激素信号的降低有关。
在扩张型心肌病小鼠模型中诱导产生心脏D3,表明D3诱导可能是对多种形式心肌病的一种普遍反应。