Why the study?
Whether enhanced inflammatory signatures in heart failure patients with CHIP derive from mutant cells or reflect systemic pro-inflammatory activation is unclear.
What are the cell-intrinsic effects of CHIP mutant cells in patients with heart failure?
Population
Patients with heart failure
Comparison
CHIP mutant cells vs wild-type cells
Design
Single-cell sequencing study
Key result
DNMT3A mutant monocytes, CD4+ T cells, and NK cells from heart failure patients exhibited significantly increased expression of genes associated with inflammation and effector functions compared to wild-type cells.
Authors
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Cell-intrinsic CHIP effects may drive HF inflammation; leaves open whether targeting mutant clones improves outcomes.
Observational (n=6)
What are the cell-intrinsic effects of CHIP mutant cells in patients with heart failure?
CHIP mutations in heart failure patients intrinsically alter immune cell gene expression, promoting inflammation and potentially explaining the worse prognosis associated with CHIP.
Abplanalp et al. (2023) conducted an observational in Heart failure with DNMT3A clonal hematopoiesis (n=6). DNMT3A mutation vs. Wild-type cells was evaluated on Differential gene expression in circulating immune cells. DNMT3A mutant monocytes, CD4+ T cells, and NK cells from heart failure patients exhibited significantly increased expression of genes associated with inflammation and effector functions compared to wild-type cells.