Neuroepithelial cell-transforming 1 promotes cardiac fibrosis via the Wnt/β-catenin signaling pathway

Bibliographic Details
Title: Neuroepithelial cell-transforming 1 promotes cardiac fibrosis via the Wnt/β-catenin signaling pathway
Authors: Tianyu Li, Xue Xiong, Yujing Wang, Yue Li, Yao Liu, Mingxiu Zhang, Chao Li, Tong Yu, Wei Cao, Shuangshuang Chen, Huizhen Zhang, Xiaona Wang, Lifang Lv, Yuhong Zhou, Haihai Liang, Xuelian Li, Hongli Shan
Source: iScience, Vol 26, Iss 10, Pp 107888- (2023)
Publisher Information: Elsevier, 2023.
Publication Year: 2023
Collection: LCC:Science
Subject Terms: Biological sciences, Biochemistry, Molecular biology, Cell biology, Science
More Details: Summary: This study found that the level of neuroepithelial cell-transforming gene 1 protein (NET1) was significantly increased in a mouse cardiac fibrosis model. Moreover, the expression level of NET1 was increased in cardiac fibrosis induced by TGF-β1, suggesting that NET1 was involved in the pathological process of cardiac fibrosis. Overexpression of NET1 promoted β-catenin expression in the nucleus and significantly increased the proliferation and migration of cardiac fibroblasts. NET1 may form a complex with β-catenin through GSK3β. Knockdown of β-catenin alleviated the effects of NET1 overexpression on collagen production and cell migration. In the heart of NET1 knockout mice, NET1 knockout can reduce the expression of β-catenin, α-SMA, and collagen content induced by MI. In conclusion, NET1 may regulate the activation of Wnt/β-catenin and TGF/Smads signaling pathway, promote collagen synthesis in fibroblasts, and participate in cardiac fibrosis. Thus, NET1 may be a potential therapeutic target in cardiac fibrosis.
Document Type: article
File Description: electronic resource
Language: English
ISSN: 2589-0042
Relation: http://www.sciencedirect.com/science/article/pii/S258900422301965X; https://doaj.org/toc/2589-0042
DOI: 10.1016/j.isci.2023.107888
Access URL: https://doaj.org/article/f288bb519999461d870559fb502d0734
Accession Number: edsdoj.f288bb519999461d870559fb502d0734
Database: Directory of Open Access Journals
More Details
ISSN:25890042
DOI:10.1016/j.isci.2023.107888
Published in:iScience
Language:English