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The LC3II/LC3I ratio and Atg5 level were upregulated by cGAS overexpression. Under calcification-inducing conditions, HDAC1 deacetylates cGAS and inactivates it. HDAC1 knockdown by short hairpin HDAC1 reversed the cGAS-induced reduction in vascular calcification, as well as in autophagy. HDAC1-induced cGAS deacetylation enhances vascular calcification and may therefore be a potential therapeutic target. HDAC1-induced cGAS deacetylation enhances vascular calcification and may therefore be a potential therapeutic target.Should theories of
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