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本文引用的文献

1
Hopx and Hdac2 interact to modulate Gata4 acetylation and embryonic cardiac myocyte proliferation.Hopx 和 Hdac2 相互作用调节 Gata4 乙酰化和胚胎心肌细胞增殖。
Dev Cell. 2010 Sep 14;19(3):450-9. doi: 10.1016/j.devcel.2010.08.012.
2
Evidence for coregulation of myocardial gene expression by MEF2 and NFAT in human heart failure.在人类心力衰竭中MEF2和NFAT对心肌基因表达进行共同调控的证据。
Circ Cardiovasc Genet. 2009 Jun;2(3):212-9. doi: 10.1161/CIRCGENETICS.108.816686. Epub 2009 Mar 31.
3
Increased cardiac myocyte progenitors in failing human hearts.衰竭的人类心脏中心肌细胞祖细胞增加。
Circulation. 2008 Aug 5;118(6):649-57. doi: 10.1161/CIRCULATIONAHA.107.761031. Epub 2008 Jul 21.
4
Transgenic overexpression of Hdac3 in the heart produces increased postnatal cardiac myocyte proliferation but does not induce hypertrophy.心脏中Hdac3的转基因过表达会使出生后心肌细胞增殖增加,但不会诱发肥大。
J Biol Chem. 2008 Sep 26;283(39):26484-9. doi: 10.1074/jbc.M803686200. Epub 2008 Jul 14.
5
Hdac2 regulates the cardiac hypertrophic response by modulating Gsk3 beta activity.组蛋白去乙酰化酶2通过调节糖原合成酶激酶3β的活性来调控心脏肥大反应。
Nat Med. 2007 Mar;13(3):324-31. doi: 10.1038/nm1552. Epub 2007 Feb 18.
6
Transcriptional genomics associates FOX transcription factors with human heart failure.转录基因组学将FOX转录因子与人类心力衰竭联系起来。
Circulation. 2006 Sep 19;114(12):1269-76. doi: 10.1161/CIRCULATIONAHA.106.632430. Epub 2006 Sep 4.
7
Regulation of cardiac hypertrophy by intracellular signalling pathways.细胞内信号通路对心肌肥大的调控
Nat Rev Mol Cell Biol. 2006 Aug;7(8):589-600. doi: 10.1038/nrm1983.
8
Mixed messages: transcription patterns in failing and recovering human myocardium.相互矛盾的信息:衰竭及恢复过程中的人类心肌转录模式
Circ Res. 2005 Mar 18;96(5):592-9. doi: 10.1161/01.RES.0000159390.03503.c3. Epub 2005 Feb 17.
9
Hopping to the beat. Hop regulation of cardiac gene expression.随节奏跳跃。心脏基因表达的跳跃调节。
Trends Cardiovasc Med. 2003 Oct;13(7):261-4. doi: 10.1016/s1050-1738(03)00107-5.
10
Myocardin mRNA is augmented in the failing myocardium: expression profiling in the porcine model and human dilated cardiomyopathy.在衰竭心肌中,心肌转录因子mRNA水平升高:猪模型和人类扩张型心肌病中的表达谱分析
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同源域仅蛋白 X 在人类心力衰竭中下调。

Homeodomain only protein x is down-regulated in human heart failure.

机构信息

Department of Cell and Developmental Biology, University of Pennsylvania, Philadelphia, PA 19104, USA.

出版信息

J Mol Cell Cardiol. 2011 Jun;50(6):1056-8. doi: 10.1016/j.yjmcc.2011.02.015. Epub 2011 Mar 5.

DOI:10.1016/j.yjmcc.2011.02.015
PMID:21382376
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3114304/
Abstract

Homeodomain only protein x (Hopx) is an unusual homeodomain protein that has diverse effects on cardiac growth. Manipulation of Hopx function in murine models is associated with cardiac hypertrophy, dilation and fibrosis. In the present study, we examined the expression profile of Hopx in various models of pathologic cardiac hypertrophy and failure. Hopx expression is significantly reduced in neonatal rat cardiac myocytes after α/β adrenergic receptor agonist treatment. Cardiac hypertrophy and failure induced by transaortic constriction in mice causes marked down-regulation of Hopx expression. Interestingly, HOPX expression was significantly reduced in hearts of humans with end-stage heart failure when compared to non-failing control hearts, and HOPX levels remain low after LVAD support. Our findings suggest that HOPX/Hopx expression is reduced in multiple examples of human and murine cardiac hypertrophy and failure.

摘要

同源域仅蛋白 X(Hopx)是一种不寻常的同源域蛋白,对心脏生长有多种影响。在鼠模型中对 Hopx 功能的操作与心脏肥大、扩张和纤维化有关。在本研究中,我们检查了 Hopx 在各种病理性心脏肥大和衰竭模型中的表达谱。α/β 肾上腺素能受体激动剂处理后,新生大鼠心肌细胞中的 Hopx 表达显著降低。转主动脉缩窄引起的小鼠心脏肥大和衰竭导致 Hopx 表达明显下调。有趣的是,与非衰竭对照心脏相比,终末期心力衰竭患者的心脏中 HOPX 表达显著降低,并且在 LVAD 支持后 HOPX 水平仍然较低。我们的发现表明,Hopx 在多种人类和鼠类心脏肥大和衰竭的模型中表达减少。