ArticleBiomolecules2026
INO80E Suppresses Oxidized LDL-Induced Endothelial Apoptosis Through HDAC1-Mediated Stabilization of YY1.
Article in Biomolecules, 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
objectivesEndothelial apoptosis is a central event in atherosclerotic vascular injury, yet the contribution of the INO80 chromatin-remodeling subunit INO80E to this process remains unclear. This study examined whether INO80E is altered during atherosclerosis (AS)-associated endothelial injury and explored its functional role in ox-LDL-triggered apoptosis.
methodsAtherosclerotic mouse models were used to examine INO80E expression in vascular tissues, and ox-LDL-treated HUVECs were applied as an in vitro model of endothelial injury. The functional role of INO80E was evaluated using lentiviral overexpression and siRNA-mediated knockdown approaches, while apoptosis was measured by flow cytometry and TUNEL staining. Mechanistic experiments included co-immunoprecipitation, immunofluorescence, YY1 acetylation analysis, and pharmacological inhibition with the pan-HDAC inhibitor trichostatin A (TSA). In addition, YY1-silencing rescue experiments were performed in INO80E-overexpressing cells to determine whether YY1 contributes to the protective effect of INO80E against ox-LDL-induced endothelial apoptosis.
resultsINO80E expression was reduced in the endothelial layer of ApoE
conclusionsThese findings suggest that INO80E protects endothelial cells from ox-LDL-induced apoptosis, at least in part by promoting HDAC-associated YY1 deacetylation and stabilization. The INO80E-HDAC1-YY1 pathway may represent a candidate protective mechanism in AS that requires further validation.
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