Science· 2017Q1
Clonal hematopoiesis associated with TET2 deficiency accelerates atherosclerosis development in mice
- 1,509citations
- Q1SCImago
- 2017year
Short summary
Mice transplanted with Tet2-deficient bone marrow cells showed accelerated atherosclerosis development compared to controls.
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Key points
- Tet2 deficiency in bone marrow cells accelerates atherosclerosis development in mice.
- Tet2-deficient macrophages secrete increased levels of interleukin-1β.
- Inflammasome activation is critical for the increased interleukin-1β secretion.
- This mechanism links epigenetic mutations in blood cells to cardiovascular disease progression.
AI-generated from the title and abstract; the full text is not read.
Abstract
Faulty blood cells and heart disease Recent studies have shown that elderly people's blood cells often harbor mutations in genes encoding certain epigenetic regulators. These mutations can lead to clonal expansion of the mutant blood cells, which increases the risk of blood cancers and cardiovascular disease. Fuster et al. generated a mouse model to investigate how one of these genes, Tet2 , affects atherosclerosis development (see the Perspective by Zhu et al. ). They found that the disease progressed more rapidly in mice transplanted with Tet2 -deficient bone marrow cells. This was due to increased secretion of interleukin-1β by Tet2 -deficient macrophages in a process that depended on the action of inflammasomes. Science , this issue p. 842 ; see also p. 798
The authors' abstract, as published at the source. Science, 2017 · DOI ↗
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Field: Hematology
HematologyMedicine