Relevant bibliographies by topics / GATA4 hypertrophy heart

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  2. Dissertations / Theses

Academic literature on the topic 'GATA4 hypertrophy heart'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "GATA4 hypertrophy heart"

1

Lu, Dan, Jizheng Wang, Jing Li, et al. "Meox1 accelerates myocardial hypertrophic decompensation through Gata4." Cardiovascular Research 114, no. 2 (2017): 300–311. http://dx.doi.org/10.1093/cvr/cvx222.

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AbstractAimsPathological hypertrophy is the result of gene network regulation, which ultimately leads to adverse cardiac remodelling and heart failure (HF) and is accompanied by the reactivation of a ‘foetal gene programme’. The Mesenchyme homeobox 1 (Meox1) gene is one of the foetal programme genes. Meox1 may play a role in embryonic development, but its regulation of pathological hypertrophy is not known. Therefore, this study investigated the effect of Meox1 on pathological hypertrophy, including familial and pressure overload-induced hypertrophy, and its potential mechanism of action.Metho
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Xiang, Fan, Yasuhiko Sakata, Lei Cui, et al. "Transcription factor CHF1/Hey2 suppresses cardiac hypertrophy through an inhibitory interaction with GATA4." American Journal of Physiology-Heart and Circulatory Physiology 290, no. 5 (2006): H1997—H2006. http://dx.doi.org/10.1152/ajpheart.01106.2005.

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Pathological cardiac hypertrophy is considered a precursor to clinical heart failure. Understanding the transcriptional regulators that suppress the hypertrophic response may have profound implications for the treatment of heart disease. We report the generation of transgenic mice that overexpress the transcription factor CHF1/Hey2 in the myocardium. In response to the α-adrenergic agonist phenylephrine, they show marked attenuation in the hypertrophic response compared with wild-type controls, even though blood pressure is similar in both groups. Isolated myocytes from transgenic mice demonst
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3

Liu, Yonggang, Man Yu, Ling Wu, and Michael T. Chin. "The bHLH transcription factor CHF1/Hey2 regulates susceptibility to apoptosis and heart failure after pressure overload." American Journal of Physiology-Heart and Circulatory Physiology 298, no. 6 (2010): H2082—H2092. http://dx.doi.org/10.1152/ajpheart.00747.2009.

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Cardiac hypertrophy is a common response to hemodynamic stress in the heart and can progress to heart failure. To investigate whether the transcription factor cardiovascular basic helix-loop-helix factor 1/hairy/enhancer of split related with YRPW motif 2 (CHF1/Hey2) influences the development of cardiac hypertrophy and progression to heart failure under conditions of pressure overload, we performed aortic constriction on 12-wk-old male wild-type (WT) and heterozygous (HET) mice globally underexpressing CHF1/Hey2. After aortic banding, WT and HET mice showed increased cardiac hypertrophy as me
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Yan, Guijun, Ni Zhu, Shengdong Huang, et al. "Orphan Nuclear Receptor Nur77 Inhibits Cardiac Hypertrophic Response to Beta-Adrenergic Stimulation." Molecular and Cellular Biology 35, no. 19 (2015): 3312–23. http://dx.doi.org/10.1128/mcb.00229-15.

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The orphan nuclear receptor Nur77 plays critical roles in cardiovascular diseases, and its expression is markedly induced in the heart after beta-adrenergic receptor (β-AR) activation. However, the functional significance of Nur77 in β-AR signaling in the heart remains unclear. By using Northern blot, Western blot, and immunofluorescent staining assays, we showed that Nur77 expression was markedly upregulated in cardiomyocytes in response to multiple hypertrophic stimuli, including isoproterenol (ISO), phenylephrine (PE), and endothelin-1 (ET-1). In a time- and dose-dependent manner, ISO incre
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Kee, Hae Jin, and Hyun Kook. "Roles and Targets of Class I and IIa Histone Deacetylases in Cardiac Hypertrophy." Journal of Biomedicine and Biotechnology 2011 (2011): 1–10. http://dx.doi.org/10.1155/2011/928326.

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Cardiac hypertrophy occurs in association with heart diseases and ultimately results in cardiac dysfunction and heart failure. Histone deacetylases (HDACs) are post-translational modifying enzymes that can deacetylate histones and non-histone proteins. Research with HDAC inhibitors has provided evidence that the class I HDACs are pro-hypertrophic. Among the class I HDACs, HDAC2 is activated by hypertrophic stresses in association with the induction of heat shock protein 70. Activated HDAC2 triggers hypertrophy by inhibiting the signal cascades of either Krüppel like factor 4 (KLF4) or inositol
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Fischer, Andreas, Jürgen Klattig, Burkhard Kneitz, et al. "Hey Basic Helix-Loop-Helix Transcription Factors Are Repressors of GATA4 and GATA6 and Restrict Expression of the GATA Target Gene ANF in Fetal Hearts." Molecular and Cellular Biology 25, no. 20 (2005): 8960–70. http://dx.doi.org/10.1128/mcb.25.20.8960-8970.2005.

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ABSTRACT The Hey basic helix-loop-helix transcription factors are downstream effectors of Notch signaling in the cardiovascular system. Mice lacking Hey2 develop cardiac hypertrophy, often associated with congenital heart defects, whereas combined Hey1/Hey2 deficiency leads to severe vascular defects and embryonic lethality around embryonic day E9.5. The molecular basis of these disorders is poorly understood, however, since target genes of Hey transcription factors in the affected tissues remain elusive. To identify genes regulated by Hey factors we have generated a conditional Hey1 knockout
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7

Li, Hui, Jin-Dong Xu, Xian-Hong Fang, et al. "Circular RNA circRNA_000203 aggravates cardiac hypertrophy via suppressing miR-26b-5p and miR-140-3p binding to Gata4." Cardiovascular Research 116, no. 7 (2019): 1323–34. http://dx.doi.org/10.1093/cvr/cvz215.

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Abstract Aims Circular RNAs (circRNAs) are involved in gene regulation in a variety of physiological and pathological processes. The present study aimed to investigate the effect of circRNA_000203 on cardiac hypertrophy and the potential mechanisms involved. Methods and results CircRNA_000203 was found to be up-regulated in the myocardium of Ang-II-infused mice and in the cytoplasma of Ang-II-treated neonatal mouse ventricular cardiomyocytes (NMVCs). Enforced expression of circRNA_000203 enhances cell size and expression of atrial natriuretic peptide and β-myosin heavy chain in NMVCs. In vivo,
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8

Gao, Si, Xue-ping Liu, Li-hua Wei, Jing Lu та Peiqing Liu. "Upregulation of α-enolase protects cardiomyocytes from phenylephrine-induced hypertrophy". Canadian Journal of Physiology and Pharmacology 96, № 4 (2018): 352–58. http://dx.doi.org/10.1139/cjpp-2017-0282.

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Cardiac hypertrophy often refers to the abnormal growth of heart muscle through a variety of factors. The mechanisms of cardiomyocyte hypertrophy have been extensively investigated using neonatal rat cardiomyocytes treated with phenylephrine. α-Enolase is a glycolytic enzyme with “multifunctional jobs” beyond its catalytic activity. Its possible contribution to cardiac dysfunction remains to be determined. The present study aimed to investigate the change of α-enolase during cardiac hypertrophy and explore its role in this pathological process. We revealed that mRNA and protein levels of α-eno
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Kim, Tae-gyun, Junqin Chen, Junich Sadoshima, and Youngsook Lee. "Jumonji Represses Atrial Natriuretic Factor Gene Expression by Inhibiting Transcriptional Activities of Cardiac Transcription Factors." Molecular and Cellular Biology 24, no. 23 (2004): 10151–60. http://dx.doi.org/10.1128/mcb.24.23.10151-10160.2004.

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ABSTRACT Mice with a homozygous knockout of the jumonji (jmj) gene showed abnormal heart development and defective regulation of cardiac-specific genes, including the atrial natriuretic factor (ANF). ANF is one of the earliest markers of cardiac differentiation and a hallmark for cardiac hypertrophy. Here, we show that JMJ represses ANF gene expression by inhibiting transcriptional activities of Nkx2.5 and GATA4. JMJ represses the Nkx2.5- or GATA4-dependent activation of the reporter genes containing the ANF promoter-enhancer or containing the Nkx2.5 or GATA4-binding consensus sequence. JMJ ph
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Lu, Chieh-Hsiang, Chia-Yao Shen, Dennis Jine-Yuan Hsieh, et al. "Deep ocean minerals inhibit IL-6 and IGFIIR hypertrophic signaling pathways to attenuate diabetes-induced hypertrophy in rat hearts." Journal of Applied Physiology 127, no. 2 (2019): 356–64. http://dx.doi.org/10.1152/japplphysiol.00184.2019.

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We previously reported that deep sea water (DSW) prolongs the life span of streptozotocin (STZ)-induced diabetic rats by the compensatory augmentation of the insulin like growth factor (IGF)-I survival signaling and inhibition of apoptosis. Here, we investigated the effects of DSW on cardiac hypertrophy in diabetic rats. Cardiac hypertrophy was induced in rats by using STZ (65 mg/kg) administered via IP injection. DSW was prepared by mixing DSW mineral extracts and desalinated water. Different dosages of DSW-1X (equivalent to 37 mg Mg2+·kg−1·day−1), 2X (equivalent to 74 mg Mg2+·kg−1·day−1) and
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Dissertations / Theses on the topic "GATA4 hypertrophy heart"

1

Whitcomb, Elizabeth Jamieson. "Identification of GATA4 Regulatory Mechanisms of Heart Development and Disease." Thesis, Université d'Ottawa / University of Ottawa, 2019. http://hdl.handle.net/10393/38830.

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The development and function of the heart is governed by a conserved set of transcription factors (TFs) that regulate gene expression in a cell-type, time point and stimulus driven manner. Of these core cardiac TFs, the most ubiquitously expressed is the zinc finger protein GATA4. In cardiomyocytes, GATA4 is central to proliferation, differentiation, hypertrophy and induction of pro-survival pathways. In cardiac endothelial cells, it is required for valve and septal development, although the exact mechanisms remain unclear. To regulate such a wide array of functions in a spatially and temporal
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Philips, Alana Sara Clinical School St George Hospital Faculty of Medicine UNSW. "Molecular insights into the biological role / mechanisms of GATA-4 and FOG-2 in normal cardiac function and in cardiac hypertrophy." Awarded by:University of New South Wales, 2007. http://handle.unsw.edu.au/1959.4/36772.

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The regulation of cardiac-specific genes such as GATA-4 and its co-factor FOG-2 is paramount for normal heart development and function. Indeed, those mechanisms that regulate GATA-4 and FOG-2 function, such as nuclear transport and the post-translational modification of SUMOylation, are of critical importance for cardiogenesis. Therefore the aims of this study were to: i) elucidate the nuclear transport mechanisms of GATA-4; ii) determine the function of SUMOylation on the biological activity of both GATA-4 and FOG-2; and iii) examine how these mechanisms impact on the role of GATA-4 and FOG-2
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Wilken, Andre. "Der Transkriptionsfaktor GATA4 und seine Rolle in der Entwicklung kardialer Hypertrophie." Doctoral thesis, 2016. http://hdl.handle.net/11858/00-1735-0000-002B-7C98-D.

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Die Rolle von GATA4 für die Entwicklung einer Hypertrophie und seine Regulation in Abhängigkeit von der Last sind im menschlichen Herzen im Gegensatz zu den zahlreichen tierexperimentellen Ansätzen bislang nicht gezielt untersucht worden. Die vorliegende Arbeit sollte zeigen, wie biomechanische Last im menschlichen Herzen die Expression von GATA4 und seine Phosphorylierung an einer aktivierenden Phosphorylierungsstelle (Serin-105) reguliert. Hierfür wurde der Einfluss eines chronischen Lastzustandes, hervorgerufen durch eine Aortenstenose, ebenso wie der eines akuten Lastzustandes durch Steig
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