ArticleCell death and differentiation2026
NAT10 regulates heart development and function by maintaining the expression of genes related to fatty acid β-oxidation and heart contraction.
Article in Cell death and differentiation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- The RNA helicase domain of NAT10 promotes the biogenesis of hypomodified ribosomes to enhance cancer cell proliferation.Nature communications · 2026Article
- The functions, mechanisms and clinical relevance of RNA and protein acetyltransferase NAT10: a comprehensive review.Cell biology and toxicology · 2026Review
- NAT10-mediated ac4C RNA acetylation stabilizes CXCL5/DEK mRNA to drive proliferation and metastasis in lung adenocarcinoma.Cell death & disease · 2026Article
- The NAT10/acCell communication and signaling : CCS · 2026Review
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Authors and funding
11 authors.
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Abstract
Energy metabolism is crucial for heart development and function, and dysregulation of this process can lead to heart failure. However, the molecular mechanisms underlying these processes, particularly the role of RNA-binding proteins (RBPs)-mediated posttranscriptional regulation, remain largely unclear. We identified N-acetyltransferase 10 (NAT10) as a key regulator of heart function and cardiac diseases. NAT10 is crucial for heart development, and its dysregulation is associated with heart failure. Cardiac-specific deletion of Nat10 leads to dilated cardiomyopathy, heart failure, and postnatal death by downregulating genes related to fatty acid β-oxidation and heart contraction. Adult-onset knockout Nat10 also results in dilated cardiomyopathy and heart failure. NAT10-deficient hiPSC-CMs also showed impaired calcium transients during contraction. Restoration of NAT10(WT) and NAT10(G641E) (an N-acetyltransferase-inactive mutation), but not NAT10(K290A) (a loss-of-RNA-binding activity mutation), fully rescues the dilated cardiomyopathy, heart failure, and postnatal death phenotypes in Nat10-CKO mice by restoring expression of genes involved in fatty acid β-oxidation and heart contraction. The RNA-binding activity of NAT10 is essential for maintaining the expression of these genes. These findings demonstrate that NAT10 plays a critical role in heart development and function by maintaining the expression of genes related to fatty acid β-oxidation and heart contraction, highlighting its importance in maintaining heart health.
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