ArticleFrontiers in pharmacology2026
Dihydromyricetin confers protection against myocardial ischemia-reperfusion injury by inhibiting ferroptosis through direct targeting of PPARα.
Article in Frontiers in pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Myocardial ischemia-reperfusion injury (MIRI) remains a therapeutic challenge with limited treatment options. Ferroptosis, characterized by lipid peroxidation, contributes significantly to MIRI pathogenesis. This study investigates whether dihydromyricetin (DHM), a bioactive flavonoid from Methods: A mouse myocardial I/R model was established Results: GSEA indicated significant activation of the ferroptosis pathway in MIRI, and cellular experiments confirmed that OGD/R induced a typical ferroptosis phenotype. DHM dose-dependently reversed OGD/R-induced ferroptosis-related alterations and ameliorated mitochondrial ultrastructural damage. Conclusion: This study demonstrates for the first time that DHM alleviates ischemia-reperfusion injury by directly targeting the E286 site of PPARα, upregulating its levels, and thereby suppressing cardiomyocyte ferroptosis. This finding reveals a novel mechanism underlying the cardioprotective effect of DHM and provides a new theoretical basis for targeting the PPARα-ferroptosis axis in MIRI intervention.
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