Abstract
Background and Aims: The thiol transferase glutaredoxin 1 controls redox signaling and cellular functions by regulating the S-glutathionylation status of critical protein thiols. Here we tested the hypothesis that by derepressing the expression of glutaredoxin 1, inhibition of histone deacetylase 2 (HDAC2) prevents nutrient stress-induced protein S-glutathionylation and monocyte dysfunction and protects against atherosclerosis.
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