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Corrigendum Open Access | 10.1172/jci.insight.187715

Tet2-mediated clonal hematopoiesis in non-conditioned mice accelerates age-associated cardiac dysfunction

Ying Wang, Soichi Sano, Yoshimitsu Yura, Zhonghe Ke, Miho Sano, Kosei Oshima, Hayato Ogawa, Keita Horitani, Kyung-Duk Min, Emiri Miura-Yura, Anupreet Kour, Megan A. Evans, María A. Zuriaga, Karen K. Hirschi, Jose J. Fuster, Eric M. Pietras, and Kenneth Walsh

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Published November 8, 2024 - More info

Published in Volume 9, Issue 21 on November 8, 2024
JCI Insight. 2024;9(21):e187715. https://doi.org/10.1172/jci.insight.187715.
© 2024 Wang et al. This work is licensed under the Creative Commons Attribution 4.0 International License. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
Published November 8, 2024 - Version history
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Related article:

Tet2-mediated clonal hematopoiesis in nonconditioned mice accelerates age-associated cardiac dysfunction
Ying Wang, … , Eric M. Pietras, Kenneth Walsh
Ying Wang, … , Eric M. Pietras, Kenneth Walsh
A model of bone marrow adoptive transfer to nonconditioned mice reveals the differential expansion kinetics of Tet2-deficient cells in immune cell populations and spontaneous age-dependent cardiomyopathy.
Research Article Aging Cardiology

Tet2-mediated clonal hematopoiesis in nonconditioned mice accelerates age-associated cardiac dysfunction

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Abstract

Clonal hematopoiesis of indeterminate potential is prevalent in elderly individuals and associated with increased risks of all-cause mortality and cardiovascular disease. However, mouse models to study the dynamics of clonal hematopoiesis and its consequences on the cardiovascular system under homeostatic conditions are lacking. We developed a model of clonal hematopoiesis using adoptive transfer of unfractionated ten-eleven translocation 2–mutant (Tet2-mutant) bone marrow cells into nonirradiated mice. Consistent with age-related clonal hematopoiesis observed in humans, these mice displayed a progressive expansion of Tet2-deficient cells in multiple hematopoietic stem and progenitor cell fractions and blood cell lineages. The expansion of the Tet2-mutant fraction was also observed in bone marrow–derived CCR2+ myeloid cell populations within the heart, but there was a negligible impact on the yolk sac–derived CCR2– cardiac-resident macrophage population. Transcriptome profiling revealed an enhanced inflammatory signature in the donor-derived macrophages isolated from the heart. Mice receiving Tet2-deficient bone marrow cells spontaneously developed age-related cardiac dysfunction characterized by greater hypertrophy and fibrosis. Altogether, we show that Tet2-mediated hematopoiesis contributes to cardiac dysfunction in a nonconditioned setting that faithfully models human clonal hematopoiesis in unperturbed bone marrow. Our data support clinical findings that clonal hematopoiesis per se may contribute to diminished health span.

Authors

Ying Wang, Soichi Sano, Yoshimitsu Yura, Zhonghe Ke, Miho Sano, Kosei Oshima, Hayato Ogawa, Keita Horitani, Kyung-Duk Min, Emiri Miura-Yura, Anupreet Kour, Megan A. Evans, Maria A. Zuriaga, Karen K. Hirschi, Jose J. Fuster, Eric M. Pietras, Kenneth Walsh

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Original citation JCI Insight. 2020;5(6):e135204. https://doi.org/10.1172/jci.insight.135204

Citation for this corrigendum: JCI Insight. 2024;9(21):e187715. https://doi.org/10.1172/jci.insight.187715

During the preparation of this manuscript, the legend for Supplemental Figure 1 was incorrectly drafted. The legend has been corrected in the the online supplemental PDF.

The authors regret the errors.

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See the related article at Tet2-mediated clonal hematopoiesis in nonconditioned mice accelerates age-associated cardiac dysfunction.

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