ArticleOxidative medicine and cellular longevity2021
Dihydrolycorine Attenuates Cardiac Fibrosis and Dysfunction by Downregulating Runx1 following Myocardial Infarction.
Article in Oxidative medicine and cellular longevity, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Targeting RUNX1 protects against diastolic dysfunction in a two-hit mouse model of heart failure with preserved ejection fraction.Cardiovascular research · 2026Article
- Runx1 drives cardiac fibrosis and heart failure through epigenetic activation of myofibroblasts in pressure overload-induced cardiac remodeling.BMC cardiovascular disorders · 2025Article
- Runt-related transcription factors: from pathogenesis to therapeutic targets in multiple-organ fibrosis.Frontiers in cell and developmental biology · 2025Review
- Brg1 and RUNX1 synergy in regulating TRPM4 channel in mouse cardiomyocytes.Frontiers in pharmacology · 2024Article
- Ribonucleicacid interference or small molecule inhibition of Runx1 in the border zone prevents cardiac contractile dysfunction following myocardial infarction.Cardiovascular research · 2023Article
- Potential traditional Chinese medicines with anti-inflammation in the prevention of heart failure following myocardial infarction.Chinese medicine · 2023Review
- Lycorine Ameliorates Thioacetamide-Induced Hepatic Fibrosis in Rats: Emphasis on Antioxidant, Anti-Inflammatory, and STAT3 Inhibition Effects.Pharmaceuticals (Basel, Switzerland) · 2022Article
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Authors and funding
4 authors.
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Abstract
In spite of early interventions to treat acute myocardial infarction (MI), the occurrence of adverse cardiac remodeling following heart failure due to acute MI remains a clinical challenge. Thus, there is an increasing demand for the development of novel therapeutic agents capable of inhibiting the development of pathological ventricular remodeling. RNA-seq data analysis of acute MI rat models from GEO revealed that Runx1 was the most differentially expressed MI-related gene. In this study, we demonstrated that increased Runx1 expression under pathological conditions results in decreased cardiac contractile function. We identified dihydrolycorine, an alkaloid lycorine, as a promising inhibitor of Runx1. Our results showed that treatment with this drug could prevent adverse cardiac remodeling, as indicated by the downregulation of fibrotic genes using western blotting (collagen I, TGF
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Registered trials
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