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扩张型心肌病中心肌对3型脱碘酶的诱导作用

Myocardial Induction of Type 3 Deiodinase in Dilated Cardiomyopathy.

作者信息

Wassner Ari J, Jugo Rebecca H, Dorfman David M, Padera Robert F, Maynard Michelle A, Zavacki Ann M, Jay Patrick Y, Huang Stephen A

机构信息

1 Thyroid Program, Division of Endocrinology, Boston Children's Hospital , Boston, Massachusetts.

2 Department of Pathology, Brigham and Women's Hospital , Boston, Massachusetts.

出版信息

Thyroid. 2017 May;27(5):732-737. doi: 10.1089/thy.2016.0570. Epub 2017 Apr 5.

DOI:10.1089/thy.2016.0570
PMID:28314380
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5421592/
Abstract

BACKGROUND

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.

METHODS

This study characterized changes in cardiac D3 and thyroid hormone signaling in a transgenic model of progressive dilated cardiomyopathy (TG9 mice).

RESULTS

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.

CONCLUSIONS

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.

摘要

背景

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。

方法

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。

结果

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。

结论

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。

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Tissue thyroid hormones and thyronamines.组织甲状腺激素和甲状腺胺。
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Executive Summary: Heart Disease and Stroke Statistics--2016 Update: A Report From the American Heart Association.执行摘要:《2016年心脏病和中风统计数据更新:美国心脏协会报告》
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Intracellular inactivation of thyroid hormone is a survival mechanism for muscle stem cell proliferation and lineage progression.甲状腺激素的细胞内失活是肌肉干细胞增殖和谱系进展的一种存活机制。
Cell Metab. 2014 Dec 2;20(6):1038-48. doi: 10.1016/j.cmet.2014.10.009. Epub 2014 Nov 13.
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Mice with hepatocyte-specific deficiency of type 3 deiodinase have intact liver regeneration and accelerated recovery from nonthyroidal illness after toxin-induced hepatonecrosis.3型脱碘酶肝细胞特异性缺乏的小鼠在毒素诱导的肝坏死发生后,具有完整的肝脏再生能力,且从非甲状腺疾病中恢复的速度加快。
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Thyroid disease and the cardiovascular system.甲状腺疾病与心血管系统。
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American Thyroid Association Guide to investigating thyroid hormone economy and action in rodent and cell models.美国甲状腺协会在啮齿动物和细胞模型中研究甲状腺激素代谢和作用的指南。
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