Critical role of VGLL4 in the regulation of chronic normobaric hypoxia-induced pulmonary hypertension in mice.


Journal

FASEB journal : official publication of the Federation of American Societies for Experimental Biology
ISSN: 1530-6860
Titre abrégé: FASEB J
Pays: United States
ID NLM: 8804484

Informations de publication

Date de publication:
08 2021
Historique:
revised: 12 07 2021
received: 04 12 2020
accepted: 15 07 2021
entrez: 27 7 2021
pubmed: 28 7 2021
medline: 5 8 2021
Statut: ppublish

Résumé

Pulmonary hypertension (PH), a rare but deadly cardiopulmonary disorder, is characterized by extensive remodeling of pulmonary arteries resulting from enhancement of pulmonary artery smooth muscle cell proliferation and suppressed apoptosis; however, the underlying pathophysiological mechanisms remain largely unknown. Recently, epigenetics has gained increasing prominence in the development of PH. We aimed to investigate the role of vestigial-like family member 4 (VGLL4) in chronic normobaric hypoxia (CNH)-induced PH and to address whether it is associated with epigenetic regulation. The rodent model of PH was established by CNH treatment (10% O

Identifiants

pubmed: 34314061
doi: 10.1096/fj.202002650RR
doi:

Substances chimiques

STAT3 Transcription Factor 0
Stat3 protein, mouse 0
Transcription Factors 0
VGLL4 protein, mouse 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

e21822

Subventions

Organisme : Zhejiang Provincial Natural Science Foundation of China
ID : LY20H010001
Organisme : Zhejiang Provincial Natural Science Foundation of China
ID : LY18H010007
Organisme : Zhejiang Provincial Natural Science Foundation of China
ID : LY17H010007
Organisme : National Natural Science Foundation of China
ID : 81900403
Organisme : National Natural Science Foundation of China
ID : 31900685

Informations de copyright

© 2021 Federation of American Societies for Experimental Biology.

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Auteurs

Qiuyun Tian (Q)

Institute of Hypoxia Medicine, School of Basic Medical Sciences, Wenzhou Medical University, Wenzhou, China.

Xiaofang Fan (X)

Institute of Hypoxia Medicine, School of Basic Medical Sciences, Wenzhou Medical University, Wenzhou, China.

Jianshe Ma (J)

Institute of Hypoxia Medicine, School of Basic Medical Sciences, Wenzhou Medical University, Wenzhou, China.

Dantong Li (D)

Institute of Hypoxia Medicine, School of Basic Medical Sciences, Wenzhou Medical University, Wenzhou, China.

Yujiao Han (Y)

Institute of Hypoxia Medicine, School of Basic Medical Sciences, Wenzhou Medical University, Wenzhou, China.

Xianghong Yin (X)

Institute of Hypoxia Medicine, School of Basic Medical Sciences, Wenzhou Medical University, Wenzhou, China.

Hui Wang (H)

Institute of Hypoxia Medicine, School of Basic Medical Sciences, Wenzhou Medical University, Wenzhou, China.

Tingting Huang (T)

Institute of Hypoxia Medicine, School of Basic Medical Sciences, Wenzhou Medical University, Wenzhou, China.

Zhenglu Wang (Z)

Renji College, Wenzhou Medical University, Wenzhou, China.

Yangping Shentu (Y)

Department of Pathology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.

Feng Xue (F)

Institute of Hypoxia Medicine, School of Basic Medical Sciences, Wenzhou Medical University, Wenzhou, China.

Congkuo Du (C)

Institute of Hypoxia Medicine, School of Basic Medical Sciences, Wenzhou Medical University, Wenzhou, China.

Yongyu Wang (Y)

Institute of Hypoxia Medicine, School of Basic Medical Sciences, Wenzhou Medical University, Wenzhou, China.

Sunzhong Mao (S)

Institute of Hypoxia Medicine, School of Basic Medical Sciences, Wenzhou Medical University, Wenzhou, China.

Junming Fan (J)

Institute of Hypoxia Medicine, School of Basic Medical Sciences, Wenzhou Medical University, Wenzhou, China.

Yongsheng Gong (Y)

Institute of Hypoxia Medicine, School of Basic Medical Sciences, Wenzhou Medical University, Wenzhou, China.

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