ArticleFrontiers in pharmacology2025
Tanshinone I promotes angiogenesis and improves ventricular remodeling post-myocardial infarction via ALDH2 signaling-mediated ferroptosis inhibition.
Article in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Programmed Cell Death of Endothelial Cells in Ischemic Heart Disease: Mechanism and Potential Cell and Gene Therapeutic Prospects.Bioengineering (Basel, Switzerland) · 2026Review
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Authors and funding
11 authors.
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Abstract
Background: Tanshinone I (Tan I) has diverse cardioprotective effects, including improving post-myocardial infarction (MI) ventricular remodeling. Ventricular remodeling can be improved by inhibiting endothelial cell (EC) ferroptosis to promote post-MI angiogenesis, but how Tan I does this remains unclear. Thus, we investigated how EC ferroptosis mediates post-MI angiogenesis and Tan I's role in this process. Methods: Results: 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 Conclusion: Tan I may improve ventricular remodeling by activating ALDH2 signaling, inhibiting EC ferroptosis, and promoting angiogenesis.
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