Tet2-Mediated Clonal Hematopoiesis Accelerates Heart Failure Through a Mechanism Involving the IL-1β/NLRP3 Inflammasome
Open accessAbstract
Background Recent studies have shown that hematopoietic stem cells can undergo clonal expansion secondary to somatic mutations in leukemia-related genes, thus leading to an age-dependent accumulation of mutant leukocytes in the blood. This somatic mutation-related clonal hematopoiesis is common in healthy older individuals, but it has been associated with an increased incidence of future cardiovascular disease. The epigenetic regulator TET2 is frequently mutated in blood cells of individuals exhibiting clonal hematopoiesis.Objectives This study investigated whether Tet2 mutations within hematopoietic cells can contribute to heart failure in 2 models of cardiac injury.Methods Heart failure was induced in mice by pressure overload, achieved by transverse aortic constriction or chronic ischemia induced by the permanent ligation of the left anterior descending artery. Competitive bone marrow transplantation strategies with Tet2-deficient cells were used to mimic TET2 mutation-driven clonal hematopoiesis. Alternatively, Tet2 was specifically ablated in myeloid cells using Cre recombinase expressed from the LysM promoter.Results In both experimental heart failure models, hematopoietic or myeloid Tet2 deficiency worsened cardiac remodeling and function, in parallel with increased interleukin-1beta (IL-1β) expression. Treatment with a selective NLRP3 inflammasome inhibitor protected against the development of heart failure and eliminated the differences in cardiac parameters between Tet2-deficient and wild-type mice.Conclusions Tet2 deficiency in hematopoietic cells is associated with greater cardiac dysfunction in murine models of heart failure as a result of elevated IL-1β signaling. These data suggest that individuals with TET2-mediated clonal hematopoiesis may be at greater risk of developing heart failure and respond better to IL-1β-NLRP3 inflammasome inhibition.
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In atherosclerosis, TET2-deficient macrophages overproduce pro-inflammatory cytokines, including interleukin-1β and interleukin-6, via enhanced NLRP3 inflammasome activation, which accelerates plaque instability and vascular injury.
“In the context of atherosclerosis, these cells overproduce pro-inflammatory cytokines, including interleukin-1β and interleukin-6, via enhanced NLRP3 inflammasome activation, which accelerates plaque instability and vascular injury [15,40]”
From Clonal Hematopoiesis of Indeterminate Potential as an Emerging Interdisciplinary Risk Factor in Alzheimer’s Disease: Current Evidence and Future Directions (2026) · cites this paper as [40]
The Introduction reports greater IL-1β secretion by Tet2-deficient macrophages and increased plaque size in hyperlipidemic mice, with NLRP3 inhibition reducing the plaque-size difference. The Discussion also links Tet2 to repression of LPS-induced IL-6, but does not say IL-6 overproduction occurs through NLRP3 activation. Neither passage establishes plaque instability or vascular injury; the reported atherosclerosis outcome is plaque size. (LLM, conf=0.87)
Experimental — accuracy not yet measuredIn cardiovascular models, TET2-deficient macrophages in the arterial wall adopt a hyper-inflammatory M1-like phenotype.
“this immune profile contrasts sharply with cardiovascular models, where TET2-deficient macrophages in the arterial wall adopt a hyper-inflammatory M1-like phenotype.”
From Clonal Hematopoiesis of Indeterminate Potential as an Emerging Interdisciplinary Risk Factor in Alzheimer’s Disease: Current Evidence and Future Directions (2026) · cites this paper as [40]
The Introduction (page not available) reports greater IL-1β secretion by Tet2-deficient macrophages in an atherosclerosis model, and the Discussion describes increased pro-inflammatory signaling. Neither passage establishes that macrophages in the arterial wall adopt an M1-like phenotype; this paper’s own experiments examine heart-failure models. (LLM, conf=0.87)
Experimental — accuracy not yet measuredMost CHIP mouse models rely on BM transplantation following high-dose irradiation and inevitably increased inflammatory milieus.
“Currently, most CHIP mouse models rely on BM transplantation following high-dose irradiation and inevitably increased inflammatory milieus.16,24,39”
From Aging drives <i>Tet2</i> <i>+/−</i> clonal hematopoiesis via IL-1 signaling (2023) · cites this paper as [39]
The Results describe this paper’s CHIP model as bone-marrow transplantation into lethally irradiated mice. They do not establish that most CHIP mouse models use this approach or that irradiation inevitably increases the inflammatory milieu; the reported inflammatory changes were measured after myocardial infarction in Tet2-deficient mice relative to transplanted controls. The Methods also describe a conditional myeloid-restricted model. (LLM, conf=0.86)
Experimental — accuracy not yet measuredLoss of Tet2 or Dnmt3a led to worsening heart function in a mouse model of congestive heart failure, corroborating the human genetic association.
“Subsequent studies showed that loss of Tet2 or Dnmt3a led to worsening heart function in a mouse model of congestive heart failure, corroborating the human genetic association 87,88.”
From Clonal hematopoiesis in human aging and disease (2019) · cites this paper as [88]
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“Subsequent studies showed that loss of Tet2 or Dnmt3a led to worsening heart function in a mouse model of congestive heart failure, corroborating the human genetic association (88, 89).”
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- Authors
- Sano, S., Oshima, K., Wang, Y., MacLauchlan, S., Katanasaka, Y., Sano, M., Zuriaga, M. A., Yoshiyama, M., Goukassian, D., Cooper, M. A., Fuster, J. J., & Walsh, K.
- Affiliations
- Boston University (US)
- Osaka City University (JP)
- Temple University (US)
- The University of Queensland (AU)
- Corresponding author
- Walsh, Kenneth
- ORCID
- Venue
- Journal of the American College of Cardiology
- Publisher
- Elsevier BV
- Published
- 2018-02
- Volume
- 71
- Issue
- 8
- Pages
- 875-886
- ISSN
- 0735-1097 (ISSN-L)
- PMC
- PMC5828038
- OpenAlex
- W2791529560
- Cited by
- 699
- References
- 47
- Citations by year
- 2026: 83 · 2025: 91 · 2024: 99 · 2023: 101 · 2022: 90 · 2021: 82 · 2020: 75 · 2019: 50 · 2018: 27 · 2012: 1
- FWCI
- 44.20
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Journal of the American College of Cardiology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- American Heart Association
- National Institutes of Health
- Japan Society for the Promotion of Science (16K18876, 15K08649)
- National Heart, Lung, and Blood Institute (R01HL131006, R01HL138014, R01HL126141, R01HL141256, R01HL132564)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Health Sciences › Medicine › Hematology › Acute Myeloid Leukemia Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Keywords
- clonal hematopoiesis, TET2, heart failure, IL-1β, NLRP3 inflammasome, pressure overload, myocardial ischemia, cardiac remodeling, hematopoietic stem cells, myeloid cells, inflammasome inhibitors
- MeSH terms
- NLR Family, Pyrin Domain-Containing 3 Protein, Animals, Cells, Cultured, DNA-Binding Proteins, Furans, Heart Failure, Hematopoiesis, Heterocyclic Compounds, 4 or More Rings, Indenes, Mice, Inbred C57BL, Mice, Transgenic, Proto-Oncogene Proteins, Sulfonamides, Sulfones, Mice, Knockout, Dioxygenases, Mice, Interleukin-1beta, Inflammasomes
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