BRIEF RESEARCH REPORT article
Front. Cardiovasc. Med.
Sec. Cardiovascular Biologics and Regenerative Medicine
Volume 12 - 2025 | doi: 10.3389/fcvm.2025.1633438
Transcription factor ETV1 promotes angiogenesis after myocardial infarction via activation of the VEGFA/VEGFR2/eNOS pathway
Provisionally accepted
- Shanxi Bethune Hospital, Shanxi Medical University, Taiyuan, China
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Background: In our previous study, through integrative transcriptomic and ChIP-seq analysis, we revealed that ETV1 is a potential transcription factor involved in ventricular remodeling in the early stage of MI. This study aims to investigate the regulatory roles of ETV1 and whether ETV1 regulates angiogenesis after MI.: In this study, MI model was induced by ligating the left anterior descending coronary artery. The expression of Etv1 was modulated via intramyocardial injection of adeno-associated virus serotype 9 (AAV9) with endothelial-specific promoter Icam2. Fibrosis was determined by Masson staining and apoptosis was assessed by TUNEL staining. Angiogenesis was evaluated by CD31 immunofluorescence staining. For in vitro experiments, HUVECs were transfected with ETV1 overexpression lentivirus, and wound healing and tube formation assays were performed to validate the angiogenic role of ETV1. Western blot was conducted to determine the level of angiogenetic factors and the underlying mechanisms. Results: The expression of Etv1 was decreased in the hearts of MI mice, as well as in isolated cardiac microvascular endothelial cells (CMECs). Moreover, overexpression of Etv1 alleviated the deterioration of heart function, mitigated the fibrosis, reduced apoptosis, and promoted angiogenesis after MI. Moreover, ETV1 overexpression enhanced migration and tube formation abilities of HUVECs. Mechanistically, ETV1 upregulated the expression of VEGFA, VEGFR2, and eNOS. Conclusions: In summary, Etv1 promote angiogenesis via activating VEGFA/VEGFR2/eNOS pathway after MI, which further ameliorate adverse ventricular remodeling. These results suggest that ETV1 may serve as a potential target for the treatment of myocardial infarction.
Keywords: Myocardial Infarction, Ventricular Remodeling, ETV1, Angiogenesis, VEGF/ VEGFR2/eNOS pathway
Received: 22 May 2025; Accepted: 05 Aug 2025.
Copyright: © 2025 Wang, Li, Li, Fang and Chen. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Yuan Chen, Shanxi Bethune Hospital, Shanxi Medical University, Taiyuan, China
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