ArticleBlood2023
Aging drives Tet2+/- clonal hematopoiesis via IL-1 signaling.
Article in Blood, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 111 papers.
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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
111 citing papers in PubMed, 138 citations in OpenAlex.
- Colchicine and Longitudinal Dynamics of Clonal Hematopoiesis: An Exploratory Substudy of the LoDoCo2 Trial.Journal of the American College of Cardiology · 2025Trial
- Effects of IL-1β inhibition on anemia and clonal hematopoiesis in the randomized CANTOS trial.Blood advances · 2023Trial
- Second primary cancers following hematologic malignancies: Epidemiology, pathobiology and clinical management.Human vaccines & immunotherapeutics · 2026Review
- Inflammation as a central driver in AML pathogenesis and therapy resistance.Science China. Life sciences · 2026Review
- Cardio-Oncological Sequelae of Autologous Stem Cell Transplantation: Role of Clonal Hematopoiesis in Cardiovascular Risk.JACC. Advances · 2026Article
- Exacerbation of inflammatory bone loss in TET2-driven clonal hematopoiesis.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- TET2 as a Context-Dependent Epigenetic Integrator in Clonal Hematopoiesis, Inflammation, Cancer, and Immunotherapy.Cell biochemistry and function · 2026Review
- Is clonal haematopoiesis the missing link between lupus and cardiovascular disease?Rheumatology (Oxford, England) · 2026Review
- Inhibition of DNA demethylation attenuates experimental necrotizing enterocolitis via suppression of TLR4-mediated inflammation.Research square · 2026Article
- Article
- Clonal hematopoiesis of indeterminate potential (CHIP)-a pivotal contributor of aging and related disorders.Annals of translational medicine · 2026Review
- Adverse Early-Life Factors Associated with Clonal Hematopoiesis of Indeterminate Potential in Later Life.Biomedicines · 2026Article
- Current Understanding of CHIP's Immunobiological Footprint with A Focus on Gastrointestinal Disorders: A Review of the Literature.Current oncology reports · 2026Review
- Engineering bone marrow in a dish-a bloody business: preclinical opportunities, translational use cases, and a call for consensus.Journal of thrombosis and haemostasis : JTH · 2026Review
- Mutant neutrophils and NETosis in clonal hematopoiesis: an emerging contributor of thromboinflammation and organ dysfunction.Journal of thrombosis and thrombolysis · 2026Review
- From complexity to clarity: aging bone marrow niche in bone and blood regeneration and malignancy.Bone research · 2026Review
- Inflammageing and clonal haematopoiesis interplay and their impact on human disease.Nature reviews. Molecular cell biology · 2026Review
- Clonal hematopoiesis and its progression to myeloid neoplasms: insights into risk, biology, and therapeutic strategies.Haematologica · 2026Review
- Oridonin as a novel KDM5C inhibitor alleviates clonal hematopoiesis-induced cardiac agingActa pharmaceutica Sinica. B · 2026Article
- TET2 loss enhances early response to inflammation in primitive and committed myeloid cells.Experimental hematology · 2026Article
51 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Clonal hematopoiesis of indeterminate potential (CHIP), also referred to as aging-related clonal hematopoiesis, is defined as an asymptomatic clonal expansion of mutant mature hematopoietic cells in ≥4% of blood leukocytes. CHIP associates with advanced age and increased risk for hematological malignancy, cardiovascular disease, and all-cause mortality. Loss-of-function somatic mutations in TET2 are frequent drivers of CHIP. However, the contribution of aging-associated cooperating cell-extrinsic drivers, like inflammation, remains underexplored. Using bone marrow (BM) transplantation and newly developed genetic mosaicism (HSC-SCL-Cre-ERT; Tet2+/flox; R26+/tm6[CAG-ZsGreen1]Hze) mouse models of Tet2+/-driven CHIP, we observed an association between increased Tet2+/- clonal expansion and higher BM levels of the inflammatory cytokine interleukin-1 (IL-1) upon aging. Administration of IL-1 to mice carrying CHIP led to an IL-1 receptor 1 (IL-1R1)-dependent expansion of Tet2+/- hematopoietic stem and progenitor cells (HSPCs) and mature blood cells. This expansion was caused by increased Tet2+/- HSPC cell cycle progression, increased multilineage differentiation, and higher repopulation capacity compared with their wild-type counterparts. In agreement, IL-1α-treated Tet2+/- hematopoietic stem cells showed increased DNA replication and repair transcriptomic signatures and reduced susceptibility to IL-1α-mediated downregulation of self-renewal genes. More important, genetic deletion of IL-1R1 in Tet2+/- HPSCs or pharmacologic inhibition of IL-1 signaling impaired Tet2+/- clonal expansion, establishing the IL-1 pathway as a relevant and therapeutically targetable driver of Tet2+/- CHIP progression during aging.
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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.