ArticleFrontiers in molecular biosciences2026
Targeting senescence-associated secretory phenotype macrophage: apigenin inhibits DOT1L-dependent H3K79me2 at
Article in Frontiers in molecular biosciences, 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
Introduction: Apigenin (API) has been utilized in the treatment of atherosclerosis. Senescent macrophages exhibit a senescence-associated secretory phenotype (SASP), which plays a critical role in the progression of atherosclerosis. Methods: Macrophages were treated with different concentrations of API. The expression of DOT1-like histone lysine methyltransferase (DOT1L) was manipulated in macrophages. Stimulation with lipopolysaccharide (LPS) was conducted to induce the SASP. Macrophage senescence was detected by senescence-associated-β-galactosidase staining. The expressions of interleukin 1 α ( Results: API treatment effectively reduced cellular senescence in LPS-exposed macrophages. Furthermore, it downregulated markers associated with senescence, SASP, and inflammation, while upregulating the anti-inflammatory cytokine IL-10. Moreover, LPS-induced DOT1L and H3K79me2 enrichment at the Conclusion: API inhibits DOT1L-mediated H3K79me2 enrichment to downregulate
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