ArticleExperimental and therapeutic medicine2022
Natural emodin reduces myocardial ischemia/reperfusion injury by modulating the RUNX1/miR‑142‑3p/DRD2 pathway and attenuating inflammation.
Article in Experimental and therapeutic medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 7 citations in OpenAlex.
- In-vivo Antioxidant Effects of Emodin on Ischemia-Reperfusion Injury of Rat's Skeletal Muscle.Drug design, development and therapy · 2026Article
- DEL-1 Protects the Myocardium From Ischemia/Hypoxia Injury Through Regulating the Sirt1/NF-κB Signaling Pathway.Immunity, inflammation and disease · 2025Article
- Advances in the pharmacological effects and molecular mechanisms of emodin in the treatment of metabolic diseases.Frontiers in pharmacology · 2023Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute myocardial infarction is one of the leading causes of death worldwide. Although timely reperfusion could attenuate myocardial ischemia injury and reduce mortality, it causes severe secondary injury to the myocardium known as myocardial ischemia/reperfusion injury (MIRI) with unmet clinical needs. Emodin has a protective effect on MIRI in rodents. However, the precise mechanism underlying its pharmacological effect remains poorly understood. Accordingly, the present study used mRNA and microRNA (miRNA) sequencing based on MIRI mouse models to determine the mechanism involved. Emodin was found to prevent MIRI and attenuate the inflammation of myocardium in the MIRI model. In addition, by using an interdisciplinary approach, the present study uncovered that emodin suppressed the runt-related transcription factor 1 (RUNX1), which is a transcription factor of miR-142-3p, in either MIRI or the hypoxia/reoxygenation injury model. Furthermore, miR-142-3p can negatively regulate dopamine receptor D2 (DRD2), which acted as an anti-inflammatory factor to suppress NF-κB-dependent inflammation and prevent MIRI. These results were demonstrated by both cellular hypoxia/reoxygenation and mouse MIRI models. Overall, the present study provided an unrevealed molecular mechanism for emodin function. Emodin could inhibit NF-κB-triggered inflammation in MIRI by regulating the RUNX1/miR-142-3p/DRD2 pathway. Therefore, the RUNX1/miR-142-3p/DRD2 pathway presented a novel target for MIRI treatment, and the application of emodin in clinical practice may improve the treatment of MIRI.
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