ArticleMolecular medicine (Cambridge, Mass.)2025
AEOL-induced NRF2 activation and DWORF overexpression mitigate myocardial I/R injury.
Article in Molecular medicine (Cambridge, Mass.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 4 papers.
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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
4 citing papers in PubMed.
- Shenqi Granules Enhance Recovery from Myocardial Ischemia-Reperfusion Injury by Downregulating MMP9 and ADH1C.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Correction: AEOL-induced NRF2 activation and DWORF overexpression mitigate myocardial I/R injury.Molecular medicine (Cambridge, Mass.) · 2026Article
- Revisiting noncoding RNAs: emerging coding functions and their impact on skeletal muscle development.Experimental & molecular medicine · 2026Review
- Microprotein, macro-effect: DWORF as a therapeutic strategy in heart failure.Frontiers in cell and developmental biology · 2026Review
Corrections and comments
- Erratum issued
Authors and funding
10 authors.
Funding
Abstract
backgroundThe causal relationship between the activation of nuclear factor erythroid 2-related factor 2 (NRF2) and the preservation of SERCA2a function in mitigating myocardial ischemia-reperfusion (mI/R) injury, along with the associated regulatory mechanisms, remains incompletely understood. This study aims to unravel how NRF2 directly or indirectly influences SERCA2a function and its regulators, phospholamban (PLN) and Dwarf Open Reading Frame (DWORF), by testing the pharmacological repositioning of AEOL-10150 (AEOL) in the context of mI/R injury.
methodsC57BL6/J, Nrf2 knockout (Nrf2
resultsIn the early stages of mI/R injury, AEOL administration reduced mitochondrial ROS production, decreased myocardial infarct size, and improved cardiac function. These effects were due to NRF2 activation, leading to the overexpression of the micro-peptide DWORF, consequently enhancing SERCA2a activity. The cardioprotective effect induced by AEOL was diminished in Nrf2
conclusionsTaken together, our study reveals that AEOL-induced NRF2-mediated overexpression of DWORF enhances myocardial function through the activation of the SERCA2a offering promising therapeutic avenues for mI/R injury.
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