Histone lysine dimethyl-demethylase KDM3A controls pathological cardiac hypertrophy and fibrosis

Histone lysine demethylases (KDMs) can mediate transcriptional reprogramming in disease states. Here the authors show that KDM3A promotes left ventricular hypertrophy and cardiac fibrosis by activating the transcription of Timp1, and that pharmacological inhibition of KDM3A attenuates cardiac remode...

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Autores principales: Qing-Jun Zhang, Tram Anh T. Tran, Ming Wang, Mark J. Ranek, Kristen M. Kokkonen-Simon, Jason Gao, Xiang Luo, Wei Tan, Viktoriia Kyrychenko, Lan Liao, Jianming Xu, Joseph A. Hill, Eric N. Olson, David A. Kass, Elisabeth D. Martinez, Zhi-Ping Liu
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Lenguaje:EN
Publicado: Nature Portfolio 2018
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Acceso en línea:https://doaj.org/article/7518fe10d5ab4b61a96ce3487b11c73b
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spelling oai:doaj.org-article:7518fe10d5ab4b61a96ce3487b11c73b2021-12-02T16:49:31ZHistone lysine dimethyl-demethylase KDM3A controls pathological cardiac hypertrophy and fibrosis10.1038/s41467-018-07173-22041-1723https://doaj.org/article/7518fe10d5ab4b61a96ce3487b11c73b2018-12-01T00:00:00Zhttps://doi.org/10.1038/s41467-018-07173-2https://doaj.org/toc/2041-1723Histone lysine demethylases (KDMs) can mediate transcriptional reprogramming in disease states. Here the authors show that KDM3A promotes left ventricular hypertrophy and cardiac fibrosis by activating the transcription of Timp1, and that pharmacological inhibition of KDM3A attenuates cardiac remodeling induced by pressure overload.Qing-Jun ZhangTram Anh T. TranMing WangMark J. RanekKristen M. Kokkonen-SimonJason GaoXiang LuoWei TanViktoriia KyrychenkoLan LiaoJianming XuJoseph A. HillEric N. OlsonDavid A. KassElisabeth D. MartinezZhi-Ping LiuNature PortfolioarticleScienceQENNature Communications, Vol 9, Iss 1, Pp 1-12 (2018)
institution DOAJ
collection DOAJ
language EN
topic Science
Q
spellingShingle Science
Q
Qing-Jun Zhang
Tram Anh T. Tran
Ming Wang
Mark J. Ranek
Kristen M. Kokkonen-Simon
Jason Gao
Xiang Luo
Wei Tan
Viktoriia Kyrychenko
Lan Liao
Jianming Xu
Joseph A. Hill
Eric N. Olson
David A. Kass
Elisabeth D. Martinez
Zhi-Ping Liu
Histone lysine dimethyl-demethylase KDM3A controls pathological cardiac hypertrophy and fibrosis
description Histone lysine demethylases (KDMs) can mediate transcriptional reprogramming in disease states. Here the authors show that KDM3A promotes left ventricular hypertrophy and cardiac fibrosis by activating the transcription of Timp1, and that pharmacological inhibition of KDM3A attenuates cardiac remodeling induced by pressure overload.
format article
author Qing-Jun Zhang
Tram Anh T. Tran
Ming Wang
Mark J. Ranek
Kristen M. Kokkonen-Simon
Jason Gao
Xiang Luo
Wei Tan
Viktoriia Kyrychenko
Lan Liao
Jianming Xu
Joseph A. Hill
Eric N. Olson
David A. Kass
Elisabeth D. Martinez
Zhi-Ping Liu
author_facet Qing-Jun Zhang
Tram Anh T. Tran
Ming Wang
Mark J. Ranek
Kristen M. Kokkonen-Simon
Jason Gao
Xiang Luo
Wei Tan
Viktoriia Kyrychenko
Lan Liao
Jianming Xu
Joseph A. Hill
Eric N. Olson
David A. Kass
Elisabeth D. Martinez
Zhi-Ping Liu
author_sort Qing-Jun Zhang
title Histone lysine dimethyl-demethylase KDM3A controls pathological cardiac hypertrophy and fibrosis
title_short Histone lysine dimethyl-demethylase KDM3A controls pathological cardiac hypertrophy and fibrosis
title_full Histone lysine dimethyl-demethylase KDM3A controls pathological cardiac hypertrophy and fibrosis
title_fullStr Histone lysine dimethyl-demethylase KDM3A controls pathological cardiac hypertrophy and fibrosis
title_full_unstemmed Histone lysine dimethyl-demethylase KDM3A controls pathological cardiac hypertrophy and fibrosis
title_sort histone lysine dimethyl-demethylase kdm3a controls pathological cardiac hypertrophy and fibrosis
publisher Nature Portfolio
publishDate 2018
url https://doaj.org/article/7518fe10d5ab4b61a96ce3487b11c73b
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