ArticleNature communications2018
Targeting of NAT10 enhances healthspan in a mouse model of human accelerated aging syndrome.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 120 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
120 citing papers in PubMed, 211 citations in OpenAlex.
- NAT10 governs development through the Xrp1-mediated stress response rather than its RNA acetylation activity.Science advances · 2026Article
- NAT10 aggravates psoriasis by promoting keratinocytes fatty acid synthesis via stable FASN transcription.Journal of pharmaceutical analysis · 2026Article
- NAT10 inhibition corrects nuclear defects in tau mutant human neurons and extends lifespan in aiScience · 2026Article
- Adipocyte-derived β-hydroxybutyrate confers metabolic resilience in multiple myeloma.Nature communications · 2026Article
- The RNA helicase domain of NAT10 promotes the biogenesis of hypomodified ribosomes to enhance cancer cell proliferation.Nature communications · 2026Article
- Targeting NAT10 with Remodelin reshapes the pro-fibrotic microenvironment in renal fibrogenesisActa pharmaceutica Sinica. B · 2026Article
- The functions, mechanisms and clinical relevance of RNA and protein acetyltransferase NAT10: a comprehensive review.Cell biology and toxicology · 2026Review
- The impact of psuedouridine modification on human tRNA.Biochemical Society transactions · 2026Review
- NAT10-dependent NCell reports · 2026Article
- NAT10-mediated acCellular & molecular biology letters · 2026Article
- Integrated epigenetic networks in aging: from histone to RNA modifications.Journal of translational medicine · 2026Review
- CRISPR-mediated targeting of theMolecular therapy. Advances · 2026Article
- The NAT10/acCell communication and signaling : CCS · 2026Review
- Targeting NAT10 alleviates colonic senescence and elderly-onset colitis by disrupting N4-acetylation of DYRK1A.Nature communications · 2026Article
- NAT10-Mediated ac4C-Modification Exacerbates Ferroptosis by Stabilizing HMOX1 in Deep Vein Thrombosis.Arteriosclerosis, thrombosis, and vascular biology · 2026Article
- NAT10 regulates heart development and function by maintaining the expression of genes related to fatty acid β-oxidation and heart contraction.Cell death and differentiation · 2026Article
- NAT10 drives hepatocellular carcinoma progression through SQLE-mediated cholesterol biosynthesis and is targetable by remodelin.iScience · 2026Article
- NAT10 Promotes Tubular Epithelial Cell Senescence in Cisplatin-Induced Acute Kidney Injury by Regulating DDX17.International journal of biological sciences · 2026Article
- Tubular NAT10 Promotes the Secretion of TGF-β and Lactate to Drive Fibroblast Activation in Diabetic Kidney Disease.International journal of biological sciences · 2026Article
- Development and Validation of an UPLC-MS/MS Method for Remodelin Quantification in Mouse Plasma and Tissues: Application to Biodistribution and Ultrastructural Assessment.Journal of analytical methods in chemistry · 2026Article
60 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
18 authors at 7 institutions in 3 countries.
Funding
Abstract
Hutchinson-Gilford Progeria Syndrome (HGPS) is a rare, but devastating genetic disease characterized by segmental premature aging, with cardiovascular disease being the main cause of death. Cells from HGPS patients accumulate progerin, a permanently farnesylated, toxic form of Lamin A, disrupting the nuclear shape and chromatin organization, leading to DNA-damage accumulation and senescence. Therapeutic approaches targeting farnesylation or aiming to reduce progerin levels have provided only partial health improvements. Recently, we identified Remodelin, a small-molecule agent that leads to amelioration of HGPS cellular defects through inhibition of the enzyme N-acetyltransferase 10 (NAT10). Here, we show the preclinical data demonstrating that targeting NAT10 in vivo, either via chemical inhibition or genetic depletion, significantly enhances the healthspan in a Lmna
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.