ArticleNature communications2024
DNMT3A clonal hematopoiesis-driver mutations induce cardiac fibrosis by paracrine activation of fibroblasts.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 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
51 citing papers in PubMed, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.
- Association of clonal haematopoiesis with heart failure incidence and outcomes: A systematic review and meta-analysis.European journal of heart failure · 2025Pooled it
- Mutations in CHIP-associated genes at myeloid neoplasm diagnosis and risk of cardiovascular/cerebrovascular events.Annals of medicine · 2026Article
- Clonal Hematopoiesis of Indeterminate Potential Proteomic Risk Score for Predicting Clinical Outcome in Patients With Heart Failure With Preserved Ejection Fraction.Circulation. Heart failure · 2026Article
- Is clonal haematopoiesis the missing link between lupus and cardiovascular disease?Rheumatology (Oxford, England) · 2026Review
- Hematopoietic mosaic chromosomal alterations are pleiotropic drivers of inflammaging, multimorbidity, and mortality.medRxiv : the preprint server for health sciences · 2026Article
- Clonal Hematopoiesis and Type 2 Diabetes: A Narrative Review.Journal of diabetes · 2026Review
- Inflammageing and clonal haematopoiesis interplay and their impact on human disease.Nature reviews. Molecular cell biology · 2026Review
- Fecal microbiota transplantation mitigates cardiac remodeling and functional impairment in mice with chronic colitis.American journal of physiology. Gastrointestinal and liver physiology · 2026Article
- Review
- Clonal Hematopoiesis in HIV and Atherosclerosis, Arterial Inflammation, and Lymph Node Metabolic Activity.medRxiv : the preprint server for health sciences · 2026Article
- Relevance of Clonal Hematopoiesis in Immune Cells for Degenerative Aortic Valve Stenosis.Journal of the American Heart Association · 2026Review
- Molecular Mechanisms of Cardiac Fibrosis: A Pathologist's Perspective.Current issues in molecular biology · 2026Review
- Emerging Mechanisms and Therapeutic Strategies in Dilated Cardiomyopathy.Biomedicines · 2026Review
- Clonal Haematopoiesis in Type 2 Diabetes: A Review of Mechanistic Links With Inflammation and Cardiovascular Disease.Diabetes/metabolism research and reviews · 2026Review
- Clonal Hematopoiesis and Incident Heart Failure.JAMA cardiology · 2026Article
- Epigenetic alterations in Myeloid Malignancies.Advances in experimental medicine and biology · 2026Review
- Cellular Senescence, Inflammaging and Cardiovascular Disease.Immunological reviews · 2026Review
- Recent advances in biomarkers for cardiac fibrosis.Frontiers in cardiovascular medicine · 2026Review
- The Immunological Consequences of Clonal Hematopoiesis in Heart Failure.Immunological reviews · 2026Review
- Prognostic significance of somatic mutations in myeloid cells of men with chronic heart failure - interaction between loss of Y chromosome and clonal haematopoiesis.European journal of heart failure · 2025Article
Corrections and comments
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Authors and funding
22 authors at 3 institutions in 1 country.
Funding
Abstract
Hematopoietic mutations in epigenetic regulators like DNA methyltransferase 3 alpha (DNMT3A), play a pivotal role in driving clonal hematopoiesis of indeterminate potential (CHIP), and are associated with unfavorable outcomes in patients suffering from heart failure (HF). However, the precise interactions between CHIP-mutated cells and other cardiac cell types remain unknown. Here, we identify fibroblasts as potential partners in interactions with CHIP-mutated monocytes. We used combined transcriptomic data derived from peripheral blood mononuclear cells of HF patients, both with and without CHIP, and cardiac tissue. We demonstrate that inactivation of DNMT3A in macrophages intensifies interactions with cardiac fibroblasts and increases cardiac fibrosis. DNMT3A inactivation amplifies the release of heparin-binding epidermal growth factor-like growth factor, thereby facilitating activation of cardiac fibroblasts. These findings identify a potential pathway of DNMT3A CHIP-driver mutations to the initiation and progression of HF and may also provide a compelling basis for the development of innovative anti-fibrotic strategies.
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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.