ArticleNature cardiovascular research2023
Loss-of-function mutations in Dnmt3a and Tet2 lead to accelerated atherosclerosis and concordant macrophage phenotypes.
Article in Nature cardiovascular research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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.
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Who cites it
84 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Association of clonal haematopoiesis with heart failure incidence and outcomes: A systematic review and meta-analysis.European journal of heart failure · 2025Pooled it
- Exercise intensity and training alter the innate immune cell type and chromosomal origins of circulating cell-free DNA in humans.Proceedings of the National Academy of Sciences of the United States of America · 2025Trial
- Resolving the links between efferocytosis and DNMT3A mutation-driven clonal hematopoiesis in atherosclerosis.The Journal of clinical investigation · 2026Article
- Efferocytosis activates a DNMT3A-mediated oxidized DNA repair pathway to enable tissue resolution.The Journal of clinical investigation · 2026Article
- Clonal hematopoiesis of indeterminate potential (CHIP), vascular somatic mutation, and cardiovascular disease: A narrative review.Vascular medicine (London, England) · 2026Review
- Article
- Clonal hematopoiesis-associated DNMT3A mutations derepress bivalent Polycomb target genes and enhance macrophage migration.bioRxiv : the preprint server for biology · 2026Article
- Retrotransposable element derepression distinguishes DNMT3A-mutant from TET2-mutant clonal haematopoiesis.GeroScience · 2026Article
- Germline and somatic variants in DNMT3A and other clonal haematopoiesis of indeterminate potential genes contribute to pulmonary arterial hypertension.European heart journal · 2026Article
- Mouse Models of Atherosclerosis: What They Teach Us, What They Miss, and When to Use Them.Bioengineering (Basel, Switzerland) · 2026Review
- Inflammation in atherosclerosis: Drivers, mechanisms and therapies.Acta pharmaceutica Sinica. B · 2026Review
- Statin Use and Genetically Predicted HMG-CoA Reductase Inhibition in Relation to Clonal Hematopoiesis.medRxiv : the preprint server for health sciences · 2026Article
- Emerging Roles for Metabolism in Myocardial Inflammation During Heart Failure.Immunological reviews · 2026Review
- Article
- Clonal hematopoiesis of indeterminate potential (CHIP)-a pivotal contributor of aging and related disorders.Annals of translational medicine · 2026Review
- Epigenetic regulation in atherosclerosis and its therapeutic potential.Nature reviews. Cardiology · 2026Review
- Immunosenescence in systemic and multi-organ aging: mechanisms, inter-organ crosstalk, and translational opportunities.npj aging · 2026Review
- Clonal haematopoiesis and cardiovascular disease, defining risk, filling gaps, and framing the future.NPJ cardiovascular health · 2026Review
- Macrophage polarization-related genes with potential causal roles in osteoporosis: a multi-omics Mendelian randomization study.Journal of orthopaedic surgery and research · 2026Article
- Novel and emerging therapeutic strategies for clonal hematopoiesis.Haematologica · 2026Review
24 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
27 authors.
Funding
Abstract
Clonal hematopoiesis of indeterminate potential (CHIP) is defined by the presence of a cancer-associated somatic mutation in white blood cells in the absence of overt hematological malignancy. It arises most commonly from loss-of-function mutations in the epigenetic regulators DNMT3A and TET2. CHIP predisposes to both hematological malignancies and atherosclerotic cardiovascular disease in humans. Here we demonstrate that loss of Dnmt3a in myeloid cells increased murine atherosclerosis to a similar degree as previously seen with loss of Tet2. Loss of Dnmt3a enhanced inflammation in macrophages in vitro and generated a distinct adventitial macrophage population in vivo which merges a resident macrophage profile with an inflammatory cytokine signature. These changes surprisingly phenocopy the effect of loss of Tet2. Our results identify a common pathway promoting heightened innate immune cell activation with loss of either gene, providing a biological basis for the excess atherosclerotic disease burden in carriers of these two most prevalent CHIP mutations.
Indexed as
Identifiers
39196062What 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.