ZYZ-168 alleviates cardiac fibrosis after myocardial infarction through inhibition of ERK1/2-dependent ROCK1 activation

Selective treatments for myocardial infarction (MI) induced cardiac fibrosis are lacking. In this study, we focus on the therapeutic potential of a synthetic cardio-protective agent named ZYZ-168 towards MI-induced cardiac fibrosis and try to reveal the underlying mechanism. ZYZ-168 was administered...

Full description

Bibliographic Details
Main Authors: Luo, Shanshan, Hieu, Tran Ba, Ma, Fenfen, Yu, Ying, Cao, Zhonglian, Wang, Minjun, Wu, Weijun, Mao, Yicheng, Rose, Peter, Law, Betty Yuen-Kwan, Zhu, Yi Zhun
Format: Article
Published: Nature Publishing Group 2017
Online Access:https://eprints.nottingham.ac.uk/41763/
_version_ 1848796349129031680
author Luo, Shanshan
Hieu, Tran Ba
Ma, Fenfen
Yu, Ying
Cao, Zhonglian
Wang, Minjun
Wu, Weijun
Mao, Yicheng
Rose, Peter
Law, Betty Yuen-Kwan
Zhu, Yi Zhun
author_facet Luo, Shanshan
Hieu, Tran Ba
Ma, Fenfen
Yu, Ying
Cao, Zhonglian
Wang, Minjun
Wu, Weijun
Mao, Yicheng
Rose, Peter
Law, Betty Yuen-Kwan
Zhu, Yi Zhun
author_sort Luo, Shanshan
building Nottingham Research Data Repository
collection Online Access
description Selective treatments for myocardial infarction (MI) induced cardiac fibrosis are lacking. In this study, we focus on the therapeutic potential of a synthetic cardio-protective agent named ZYZ-168 towards MI-induced cardiac fibrosis and try to reveal the underlying mechanism. ZYZ-168 was administered to rats with coronary artery ligation over a period of six weeks. Ecocardiography and Masson staining showed that ZYZ-168 substantially improved cardiac function and reduced interstitial fibrosis. The expression of α–smooth muscle actin (α-SMA) and Collagen I were reduced as was the activity of matrix metalloproteinase 9 (MMP-9). These were related with decreased phosphorylation of ERK1/2 and expression of Rho-associated coiled-coil containing protein kinase 1 (ROCK1). In cardiac fibroblasts stimulated with TGF-β1, phenotypic switches of cardiac fibroblasts to myofibroblasts were observed. Inhibition of ERK1/2 phosphorylation or knockdown of ROCK1 expectedly reduced TGF-β1 induced fibrotic responses. ZYZ-168 appeared to inhibit the fibrotic responses in a concentration dependent manner, in part via a decrease in ROCK 1 expression through inhibition of the phosphorylation status of ERK1/2. For inhibition of ERK1/2 phosphorylation with a specific inhibitor reduced the activation of ROCK1. Considering its anti-apoptosis activity in MI, ZYZ-168 may be a potential drug candidate for treatment of MI-induced cardiac fibrosis.
first_indexed 2025-11-14T19:46:34Z
format Article
id nottingham-41763
institution University of Nottingham Malaysia Campus
institution_category Local University
last_indexed 2025-11-14T19:46:34Z
publishDate 2017
publisher Nature Publishing Group
recordtype eprints
repository_type Digital Repository
spelling nottingham-417632020-05-04T18:36:43Z https://eprints.nottingham.ac.uk/41763/ ZYZ-168 alleviates cardiac fibrosis after myocardial infarction through inhibition of ERK1/2-dependent ROCK1 activation Luo, Shanshan Hieu, Tran Ba Ma, Fenfen Yu, Ying Cao, Zhonglian Wang, Minjun Wu, Weijun Mao, Yicheng Rose, Peter Law, Betty Yuen-Kwan Zhu, Yi Zhun Selective treatments for myocardial infarction (MI) induced cardiac fibrosis are lacking. In this study, we focus on the therapeutic potential of a synthetic cardio-protective agent named ZYZ-168 towards MI-induced cardiac fibrosis and try to reveal the underlying mechanism. ZYZ-168 was administered to rats with coronary artery ligation over a period of six weeks. Ecocardiography and Masson staining showed that ZYZ-168 substantially improved cardiac function and reduced interstitial fibrosis. The expression of α–smooth muscle actin (α-SMA) and Collagen I were reduced as was the activity of matrix metalloproteinase 9 (MMP-9). These were related with decreased phosphorylation of ERK1/2 and expression of Rho-associated coiled-coil containing protein kinase 1 (ROCK1). In cardiac fibroblasts stimulated with TGF-β1, phenotypic switches of cardiac fibroblasts to myofibroblasts were observed. Inhibition of ERK1/2 phosphorylation or knockdown of ROCK1 expectedly reduced TGF-β1 induced fibrotic responses. ZYZ-168 appeared to inhibit the fibrotic responses in a concentration dependent manner, in part via a decrease in ROCK 1 expression through inhibition of the phosphorylation status of ERK1/2. For inhibition of ERK1/2 phosphorylation with a specific inhibitor reduced the activation of ROCK1. Considering its anti-apoptosis activity in MI, ZYZ-168 may be a potential drug candidate for treatment of MI-induced cardiac fibrosis. Nature Publishing Group 2017-03-07 Article PeerReviewed Luo, Shanshan, Hieu, Tran Ba, Ma, Fenfen, Yu, Ying, Cao, Zhonglian, Wang, Minjun, Wu, Weijun, Mao, Yicheng, Rose, Peter, Law, Betty Yuen-Kwan and Zhu, Yi Zhun (2017) ZYZ-168 alleviates cardiac fibrosis after myocardial infarction through inhibition of ERK1/2-dependent ROCK1 activation. Scientific Reports, 7 . 43242/1-43242/14. ISSN 2045-2322 http://www.nature.com/articles/srep43242 doi:10.1038/srep43242 doi:10.1038/srep43242
spellingShingle Luo, Shanshan
Hieu, Tran Ba
Ma, Fenfen
Yu, Ying
Cao, Zhonglian
Wang, Minjun
Wu, Weijun
Mao, Yicheng
Rose, Peter
Law, Betty Yuen-Kwan
Zhu, Yi Zhun
ZYZ-168 alleviates cardiac fibrosis after myocardial infarction through inhibition of ERK1/2-dependent ROCK1 activation
title ZYZ-168 alleviates cardiac fibrosis after myocardial infarction through inhibition of ERK1/2-dependent ROCK1 activation
title_full ZYZ-168 alleviates cardiac fibrosis after myocardial infarction through inhibition of ERK1/2-dependent ROCK1 activation
title_fullStr ZYZ-168 alleviates cardiac fibrosis after myocardial infarction through inhibition of ERK1/2-dependent ROCK1 activation
title_full_unstemmed ZYZ-168 alleviates cardiac fibrosis after myocardial infarction through inhibition of ERK1/2-dependent ROCK1 activation
title_short ZYZ-168 alleviates cardiac fibrosis after myocardial infarction through inhibition of ERK1/2-dependent ROCK1 activation
title_sort zyz-168 alleviates cardiac fibrosis after myocardial infarction through inhibition of erk1/2-dependent rock1 activation
url https://eprints.nottingham.ac.uk/41763/
https://eprints.nottingham.ac.uk/41763/
https://eprints.nottingham.ac.uk/41763/