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Article Abstract
The factors that modulate the inflammatory response in atherosclerosis are not well defined. In this issue of Immunity, Asare et al. examine the impact of a cis-regulatory element (CRE) that controls expression of HDAC9 and find that HDAC9-mediated deacetylation of NLRP3 might be the mechanism by which genetic variants in this conserved CRE influence the inflammation associated with human atherosclerosis.
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| http://dx.doi.org/10.1016/j.immuni.2025.02.010 | DOI Listing |
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The CREscendoing promise of HDAC targeting to limit atherosclerosis.
Immunity
March 2025
Department of Laboratory Medicine, Medical University of Vienna, Vienna, Austria. Electronic address:
The factors that modulate the inflammatory response in atherosclerosis are not well defined. In this issue of Immunity, Asare et al. examine the impact of a cis-regulatory element (CRE) that controls expression of HDAC9 and find that HDAC9-mediated deacetylation of NLRP3 might be the mechanism by which genetic variants in this conserved CRE influence the inflammation associated with human atherosclerosis.
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