ReviewThe Journal of clinical investigation2024
Clonal hematopoiesis and atherosclerosis.
Review in The Journal of clinical investigation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.
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
37 citing papers in PubMed, 1 synthesis or guideline pooled it.
- JAK2-V617F mutation among blood donors: A meta-analysis.Saudi medical journal · 2024Pooled it
- Senescent obesity signature in breast cancer: a paradigm of reverse cardio-oncology.European heart journal · 2026Review
- Impaired Glycolysis Leads to Defective Efferocytosis and Impaired Plaque Resolution inCirculation · 2026Article
- TET2 as a Context-Dependent Epigenetic Integrator in Clonal Hematopoiesis, Inflammation, Cancer, and Immunotherapy.Cell biochemistry and function · 2026Review
- Residual cardiovascular risk in coronary artery disease: from pathophysiology to established and novel therapies.Nature reviews. Cardiology · 2026Review
- Article
- Clonal Hematopoiesis and Type 2 Diabetes: A Narrative Review.Journal of diabetes · 2026Review
- Clonal Hematopoiesis and Risk of Stroke: Evidence From Over 800 000 Individuals Across 3 Cohorts.Stroke · 2026Article
- Ligature-induced periodontitis promotesHaematologica · 2026Article
- Oridonin as a novel KDM5C inhibitor alleviates clonal hematopoiesis-induced cardiac agingActa pharmaceutica Sinica. B · 2026Article
- Inflammageing and clonal haematopoiesis interplay and their impact on human disease.Nature reviews. Molecular cell biology · 2026Review
- Clonal Hematopoiesis in HIV and Atherosclerosis, Arterial Inflammation, and Lymph Node Metabolic Activity.medRxiv : the preprint server for health sciences · 2026Article
- Clonal Hematopoiesis of Indeterminate Potential (CHIP): A Model of Mutation-Driven Thromboinflammation.Cancers · 2026Review
- Geroscience insights into difficult-to-treat rheumatoid arthritis: the role of unhealthy aging, comorbidity, and therapeutic complexity.GeroScience · 2026Review
- Reframing-renaming(?)-myelodysplastic syndromes/neoplasms and clonal hematopoiesis of indeterminate potential.Leukemia · 2026Review
- Survival in patients with monoclonal gammopathy of unknown significance after transcatheter aortic valve replacement: a global retrospective propensity-matched real-world analysis.Cardio-oncology (London, England) · 2026Article
- Single-Cell Genomics and Somatic Variation in Circulating and Cardiac Resident Cells.Circulation research · 2026Review
- Clonal hematopoiesis of indeterminate potential and cardiovascular disease: mechanistic insights, clinical implications, and the dawn of precision cardio-hematology.Frontiers in cardiovascular medicine · 2026Review
- Clonal Hematopoiesis of Indeterminate Potential in Cardiovascular Disease: Gene-Specific Mechanisms and Therapeutic Implications.International journal of general medicine · 2026Review
- Cardiovascular risk stratification in inflammatory-driven conditions: how far have we come?Frontiers in cardiovascular medicine · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
Clonal hematopoiesis of indeterminate potential (CHIP) has emerged as a previously unrecognized, potent, age-related, and common risk factor for atherosclerosis. Somatic mutations in certain known leukemia driver genes give rise to clones of mutant cells in peripheral blood. The increased risk of developing hematologic malignancy does not, on its own, explain excess mortality in individuals with CHIP. Cardiovascular disease accounts for much of this gap. Experimental evidence supports the causality of certain CHIP mutations in accelerated atherosclerosis. CHIP due to mutations in different driver genes varies in their promotion of atherosclerotic events and in the region of augmented atherosclerotic involvement. For example, CHIP due to mutations in DNMT3a appears less atherogenic than CHIP that arises from TET2 or JAK2, forms of CHIP that incite inflammation. The recognition of certain CHIP mutations as promoters of atherosclerotic risk has opened new insights into understanding of the pathophysiology of this disease. The accentuated cardiovascular risk and involvement of distinct pathways of various forms of CHIP also inform novel approaches to allocation of targeted therapies, affording a step toward personalized medicine.
Indexed as
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What Socratic 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 Socratic graph.