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...
Guardado en:
Autores principales: | , , , , , , , , , , , , , , , |
---|---|
Formato: | article |
Lenguaje: | EN |
Publicado: |
Nature Portfolio
2018
|
Materias: | |
Acceso en línea: | https://doaj.org/article/7518fe10d5ab4b61a96ce3487b11c73b |
Etiquetas: |
Agregar Etiqueta
Sin Etiquetas, Sea el primero en etiquetar este registro!
|
id |
oai:doaj.org-article:7518fe10d5ab4b61a96ce3487b11c73b |
---|---|
record_format |
dspace |
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 |
work_keys_str_mv |
AT qingjunzhang histonelysinedimethyldemethylasekdm3acontrolspathologicalcardiachypertrophyandfibrosis AT tramanhttran histonelysinedimethyldemethylasekdm3acontrolspathologicalcardiachypertrophyandfibrosis AT mingwang histonelysinedimethyldemethylasekdm3acontrolspathologicalcardiachypertrophyandfibrosis AT markjranek histonelysinedimethyldemethylasekdm3acontrolspathologicalcardiachypertrophyandfibrosis AT kristenmkokkonensimon histonelysinedimethyldemethylasekdm3acontrolspathologicalcardiachypertrophyandfibrosis AT jasongao histonelysinedimethyldemethylasekdm3acontrolspathologicalcardiachypertrophyandfibrosis AT xiangluo histonelysinedimethyldemethylasekdm3acontrolspathologicalcardiachypertrophyandfibrosis AT weitan histonelysinedimethyldemethylasekdm3acontrolspathologicalcardiachypertrophyandfibrosis AT viktoriiakyrychenko histonelysinedimethyldemethylasekdm3acontrolspathologicalcardiachypertrophyandfibrosis AT lanliao histonelysinedimethyldemethylasekdm3acontrolspathologicalcardiachypertrophyandfibrosis AT jianmingxu histonelysinedimethyldemethylasekdm3acontrolspathologicalcardiachypertrophyandfibrosis AT josephahill histonelysinedimethyldemethylasekdm3acontrolspathologicalcardiachypertrophyandfibrosis AT ericnolson histonelysinedimethyldemethylasekdm3acontrolspathologicalcardiachypertrophyandfibrosis AT davidakass histonelysinedimethyldemethylasekdm3acontrolspathologicalcardiachypertrophyandfibrosis AT elisabethdmartinez histonelysinedimethyldemethylasekdm3acontrolspathologicalcardiachypertrophyandfibrosis AT zhipingliu histonelysinedimethyldemethylasekdm3acontrolspathologicalcardiachypertrophyandfibrosis |
_version_ |
1718383285165359104 |