ArticleNature communications2025
Somatic NAP1L1 p.D349E promotes cardiac hypertrophy through cGAS-STING-IFN signaling.
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 7 papers.
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Who cites it
7 citing papers in PubMed.
- Nanoparticle-Based Targeted Drug-Delivery Systems for Cardiomyopathy: Mechanisms and Therapeutic Advances.Molecules (Basel, Switzerland) · 2026Review
- Emerging roles of the cGAS/STING pathway in cardiovascular diseases.The Journal of clinical investigation · 2026Review
- PARKIN overexpression confers cardioprotection via suppressing the mtDNA-cGAS-STING axis in myocardial ischemia/reperfusion injury.Basic research in cardiology · 2026Article
- Tectochrysin alleviates Ang II-induced pathological cardiac hypertrophy by binding to STING and inhibiting STING/NFκB-mediated inflammation.Frontiers in pharmacology · 2026Article
- The Research Progress of Tumor-Associated Macrophages in Prostate Cancer.Journal of immunology research · 2026Review
- Nucleosome assembly protein-like 1 degradation-dependent novel cardioprotection mechanism of Wnt2 against ischemia‒reperfusion injury.Signal transduction and targeted therapy · 2025Article
- Maternal monocyte-derived IFN-α1 triggers early fetal demise.Journal of translational medicine · 2025Article
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13 authors.
Funding
Abstract
Hypertrophic cardiomyopathy (HCM) is the most common inherited heart disease, often caused by sarcomere gene mutations, though many sporadic cases remain genetically unexplained. Here we show that the somatic variant NAP1L1 p.D349E was involved in cardiac hypertrophy in sporadic HCM patients. Through next generation sequencing, we found that somatic variant NAP1L1 p.D349E was recurrent in the cardiomyocytes of gene-elusive sporadic HCM patients. Subsequent in vivo and in vitro functional analysis confirmed that NAP1L1 p.D349E contributes to HCM by triggering an innate immunity response. This mutation destabilizes nucleosome formation, causing DNA to leak into the cytoplasm. This leakage activates a key immune pathway, cGAS-STING, which leads to the release of inflammatory molecules and promotes heart muscle thickening. Our findings reveal a new mechanism driving HCM and suggest that somatic variants could be important in understanding and management of HCM.
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