ArticleNature communications2025
Histone acetyltransferase 1 promotes postinfarction inflammatory response by regulation of monocyte histone succinylation.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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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Who cites it
2 citing papers in PubMed.
- Integrated epigenetic networks in aging: from histone to RNA modifications.Journal of translational medicine · 2026Review
- Monocyte-to-lymphocyte ratio as a predictor of left ventricular aneurysm in acute STEMI patients.Frontiers in endocrinology · 2025Article
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Authors and funding
12 authors.
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Abstract
Early activation and phenotypic transformation of monocytes and macrophages are essential for inflammatory activities and tissue repair following myocardial infarction (MI). However, the involvement of histone succinylation in monocyte phenotypic regulation during MI remains poorly understood. Here we show that succinylation, particularly histone H3K23succ, is significantly upregulated in monocytes from both MI patients and male mouse models, correlating with enhanced inflammatory responses. We further reveal that histone acetyltransferase 1 (Hat1) acts as a succinyltransferase essential for catalytic activity, and is upregulated together with histone succinylation in proinflammatory monocytes. Deficiency in Hat1 expression improves cardiac function, reduces infarct size, and suppresses inflammatory responses in infarcted hearts after MI. Mechanistically, Hat1 modulates chromatin accessibility and recruits H3K23 succinylation to regulate proinflammatory gene expression in monocytes and macrophages post-MI. Our study reveals a critical role for histone succinylation in early MI progression and establishes that Hat1 acts as an epigenetic regulator promoting proinflammatory monocyte transformation, highlighting its therapeutic potential for MI treatment.
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