Research Paper Volume 13, Issue 9 pp 12919—12928

Knockdown of ZFAS1 improved the cardiac function of myocardial infarction rats via regulating Wnt/β-catenin signaling pathway

Bing Zou1, *, , Tieqiu Huang1, *, , Dan Wu2, , Xiaomin Hu1, , Linghui Xiao1, , Chenxi Wang1, , Hongzhou Zhang1, , Jian Xiang1, , Chenkai Hu1, , Qinghua Wu1, , Tao Wu1, ,

  • 1 Department of Cardiovascular Medicine, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, China
  • 2 Jiangxi Health Vocational College, Nanchang, Jiangxi 330052, China
* Equal contribution

Received: February 6, 2021       Accepted: March 14, 2021       Published: May 5, 2021
How to Cite

Copyright: © 2021 Zou et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.


Myocardial infarction (MI) is a big health threat in the world, and it is characterized by high morbidity and mortality. However, current treatments are not effective enough, and novel therapeutic strategies need to be explored. ZFAS1 has been proved to be involved in the regulation of MI, but the specific mechanism remains unclear. MI rats were constructed through left anterior descending artery ligation, and hypoxia cell model was also established. The proliferation, invasion, and migration of cells were detected via CCK8, traswell, and wound healing methods. Immunohistochemistry staining, western blotting, and qRT-PCR were used to detect the levels of molecules. Knockdown of ZFAS1 significantly increased the proliferation, migration, and invasion of cardiac fibroblasts. Knockdown of ZFAS1 remarkably improved cardiac function via decreasing infarction ratio and increasing vWF expression, left ventricular ejection fraction, and left ventricular fractional shortening compared with group MI. Knockdown of ZFAS1 also suppressed Wnt/β-catenin pathway in vivo. The inhibition of Wnt/β-catenin remarkably reversed the influence of shZFAS1 on cardiac function and cardiac fibroblasts viability. Therefore, Knockdown of ZFAS1 could improve the cardiac function of myocardial infarction rats via regulating Wnt/β-catenin signaling pathway. The present study might provide new thoughts for the prevention and treatment of MI damage.


MI: Myocardial infarction; PCI: Percutaneous coronary intervention; LncRNA: Long non-coding RNA; SD: Standard deviation; SERCA2a: Sarcoplasmic reticulum Ca2+ ATPase 2A; LVEF: left ventricular ejection fraction; LVFS: left ventricular fractional shortening; PEDF: Pigment epithelium-derived factor; RT-PCR: Real-time polymerase chain reaction; HE: Hematoxylin-eosin.