ArticleFrontiers in pharmacology2026
Establishing a direct interaction between the 19,20-EDP analog SA-22 and SIRT3: impact on cardiac mitochondrial homeostasis.
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: Despite extensive study, the structural, metabolic, and mechanistic heterogeneity amongst polyunsaturated fatty acids (PUFA) have confounded identification of their molecular targets and roles in cardiovascular diseases. Previously our group demonstrated that the cardioprotective properties of both 19,20-epoxydocosapentaenoic acid (EDP), a CYP450-derived metabolite of docosahexaenoic acid (DHA), and a synthetic structural analog SA-22, were SIRT3-dependent. Thus, we explored the impact of this signaling on mitochondrial homeostasis in the context of hypoxic myocardial injury. SA-22 ligand binding was confirmed via SYPRO Orange thermal shift assay. Methodology: SIRT3 catalytic activity was measured using an acetylated HDAC fluorogenic substrate assay. Point mutagenesis experiments confirmed the involvement of residue SER149. H9c2 cells were used as an Results: Addition of SA-22 altered SYPRO Orange fluorescence and improved catalytic activity Conclusion: In conclusion, SA-22 directly binds and enhances the activity of SIRT3, preserving cardiac mitochondrial homeostasis despite myocardial hypoxia-reoxygenation injury.
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