ArticleiScience2026
NAT10 exacerbates aortic valve calcification via PCSK9 mRNA ac4C acetylation.
Article in iScience, 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
10 authors.
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Abstract
N4-acetylcytidine (ac4C) is an epitranscriptomic regulator involved in diverse pathological processes. This study investigates the role of N-acetyltransferase 10 (NAT10), the primary enzyme responsible for ac4C deposition, in aortic valve calcification (AVC). NAT10 expression and global ac4C levels are upregulated in calcified aortic valves from human patients and murine models. Clinically, elevated NAT10 expression correlates with increased disease severity. Functionally, NAT10 promotes human valvular interstitial cells (hVICs) osteogenic differentiation. In high-cholesterol diet (HCD)-fed
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