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Edaravone Attenuates Carbonyl-Stress-Driven ApoA-I Carboxymethylation and Macrophage Cholesterol-Handling Dysfunction in Diabetic Atherosclerosis
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DOI：10.1016/j.freeradbiomed.2026.07.044.png)
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Abstract
En 中文
• Site-resolved LC-MS/MS mapped glyoxal-responsive CML sites on ApoA-I. • Glyoxal-modified ApoA-I impaired macrophage cholesterol efflux. • Edaravone reduced ApoA-I CML formation under glyoxal stress. • Edaravone remodeled macrophage and endothelial states in diabetic aortas. • Carbonyl stress contributes to HDL dysfunction in diabetic atherosclerosis.
Journal
IF:
8.2
Papers:
2.1W
Citations:
5.4W
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