ORIGINAL RESEARCH article
Front. Pharmacol.
Sec. Ethnopharmacology
Volume 16 - 2025 | doi: 10.3389/fphar.2025.1601017
This article is part of the Research TopicTherapeutic Targeting of Cell Death in Cardiovascular Diseases: From Mechanisms to Clinical ApplicationsView all articles
Tanshinone I promotes angiogenesis and improves ventricular remodeling post-myocardial infarction via ALDH2 signaling-mediated ferroptosis inhibition
Provisionally accepted
Feng Zhang1Lei Li1Qian Liu1
Wen-Long Wang1Zhi-Xin Wang1Rong-Qiang Song1Jian Sun1Yi-Yi Zhang1Xin-Chen Ren1Dong Wang1
Yu-ting Wu1,2*- 1Binzhou Medical University Hospital, Binzhou, Shandong Province, China
- 2Southern Medical University, Guangzhou, China
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Tanshinone I (Tan I) possesses diverse cardioprotective effects, such as improving ventricular remodeling after myocardial infarction (MI). Ventricular remodeling can be improved through promoting post-infarction angiogenesis by inhibiting endothelial cell (EC) ferroptosis. However, the role and underlying mechanism of Tan I in improving post-infarction ventricular remodeling by inhibiting ferroptosis and promoting angiogenesis remain unclear. Therefore, the mechanism of EC ferroptosis in mediating angiogenesis post-MI and the role of Tan I in promoting angiogenesis and improving ventricular remodeling were investigated. We found that Tan I improved post-infarction cardiac function and myocardial injury, inhibited post-infarction collagen deposition and EC ferroptosis, and promoted CD31 expression in vivo by activating ALDH2 and promoting ALDH2 signaling-related protein levels (ALDH2, xCT, and GPX4). Additionally, Tan I inhibited ferroptosis, promoted proliferation and migration, and enhanced tubular network formation in HUVECs in vitro by activating ALDH2 and promoting ALDH2 signaling-related protein levels. Besides, the role of Tan I was further verified by using the ferroptosis inhibitor ferrostatin-1 (Fer-1) and the ALDH2 agonist Alda-1 or the inhibitor daidzein in vitro and in vivo, respectively. Collectively, Tan I may improve ventricular remodeling by activating ALDH2 signaling, inhibiting EC ferroptosis, and promoting angiogenesis.
Keywords: Myocardial Infarction, ferroptosis, ALDH2, Angiogenesis, Ventricular Remodeling
Received: 28 Mar 2025; Accepted: 17 Jun 2025.
Copyright: © 2025 Zhang, Li, Liu, Wang, Wang, Song, Sun, Zhang, Ren, Wang and Wu. 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: Yu-ting Wu, Southern Medical University, Guangzhou, China
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