Journal Article10.1016/J.TOX.2014.06.006
DNMT3A silencing RASSF1A promotes cardiac fibrosis through upregulation of ERK1/2.
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TL;DR: It is demonstrated that downregulation of RASSF1A is associated with cardiac fibrosis and fibroblasts activation and DNMT3A likely plays an essential role in RASSf1A mediated upregulation of ERK1/2 in rat heart fibrosis.
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About: This article is published in Toxicology. The article was published on 02 Sep 2014. The article focuses on the topics: Cardiac fibrosis & Downregulation and upregulation.
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Citations
Epigenetic Therapy for the Treatment of Hypertension-Induced Cardiac Hypertrophy and Fibrosis
Chris J Watson,Stephen Horgan,Roisin Neary,Nadezhda Glezeva,Isaac Tea,Niamh Corrigan,Kenneth McDonald,Mark Ledwidge,John A. Baugh +8 more
TL;DR: Therapeutic intervention with 5-aza demonstrated favorable effects highlighting the potential use of this epigenetic modifier as a treatment option for cardiac pathologies associated with hypertrophy and fibrosis.
Genetics and Epigenetics of Atrial Fibrillation.
TL;DR: This review aims to provide a current state of the field regarding the identification and functional characterization of AF-related epigenetic regulatory networks.
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Epigenetics and the overhealing wound: the role of DNA methylation in fibrosis
TL;DR: This review will focus on DNA methylation; its association with fibroblast differentiation and activation and the consequent buildup of fibrotic scar tissue and the potential use of therapies that modulate this epigenetic pathway for the treatment of fibrosis in several organ systems.
Epigenetics in fibrosis.
TL;DR: This review aims to examine the role of epigenetics in fibrosis, evaluating all three mechanisms, and to suggest possible areas where epigenetics could be targeted therapeutically.
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Heart Failure: Advanced Development in Genetics and Epigenetics
TL;DR: An overview of genetic mutations associated with cardiomyopathy and the roles of some epigenetic mechanisms in HF is given.
References
Dnmt3a is essential for hematopoietic stem cell differentiation.
Grant A. Challen,Deqiang Sun,Mira Jeong,Min Luo,Jaroslav Jelinek,Jonathan S. Berg,Jonathan S. Berg,Christoph Bock,Aparna Vasanthakumar,Hongcang Gu,Yuanxin Xi,Shoudan Liang,Yue Lu,Gretchen J. Darlington,Alexander Meissner,Jean Pierre J. Issa,Lucy A. Godley,Wei Li,Margaret A. Goodell +18 more
TL;DR: Using conditional ablation, it is shown that Dnmt3a loss progressively impairs hematopoietic stem cell differentiation over serial transplantation, while simultaneously expanding HSC numbers in the bone marrow.
Potential Therapeutic Targets for Cardiac Fibrosis TGFβ, Angiotensin, Endothelin, CCN2, and PDGF, Partners in Fibroblast Activation
TL;DR: Recent observations concerning the contribution of TGF, endothelin-1, angiotensin II, Ang II, CCN2, and PDGF and to fibroblast activation in tissue repair and fibrosis and the potential utility of agents blocking these proteins in affecting the outcome of cardiac fibrosis are summarized.
693
Dnmt3a-Dependent Nonpromoter DNA Methylation Facilitates Transcription of Neurogenic Genes
Hao Wu,Volkan Coskun,Jifang Tao,Wei Xie,Weihong Ge,Kazuaki Yoshikawa,En Li,Yi Zhang,Yi E. Sun,Yi E. Sun +9 more
TL;DR: Genome-wide analysis of postnatal NSCs indicates that Dnmt3a occupies and methylates intergenic regions and gene bodies flanking proximal promoters of a large cohort of transcriptionally permissive genes, many of which encode regulators of neurogenesis and may be used for maintaining active chromatin states of genes critical for development.
Methylation determines fibroblast activation and fibrogenesis in the kidney
Wibke Bechtel,Scott McGoohan,Elisabeth M. Zeisberg,Gerhard A. Müller,Hubert Kalbacher,David J. Salant,Claudia A. Müller,Raghu Kalluri,Michael Zeisberg +8 more
TL;DR: It is demonstrated here that hypermethylation of RASAL1, encoding an inhibitor of the Ras oncoprotein, is associated with the perpetuation of fibroblast activation and fibrogenesis in the kidney.
DNA methylation inhibitor 5-Aza-2'-deoxycytidine induces reversible genome-wide DNA damage that is distinctly influenced by DNA methyltransferases 1 and 3B.
TL;DR: It is demonstrated that 5-azadC treatment results in growth inhibition and G2 arrest—hallmarks of a DNA damage response, and novel functions for DNMT1 are revealed as a component of the cellular response to DNA damage, which may help optimize patient responses to this agent in the future.
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