Key result
Depleting CCR2+ macrophages prevents fibro-fatty remodeling, atrial dilation, and AF in obese mice.
Why the study?
Inflammation is associated with atrial fibrillation, but its precise impact on the long-term progression of the atrial fibrillation substrate, or atrial cardiomyopathy, remains debated.
Does macrophage depletion prevent fibro-fatty remodeling and atrial fibrillation in a mouse model of obesity and atrial cardiomyopathy?
Does macrophage depletion prevent fibro-fatty remodeling and atrial fibrillation in a mouse model of obesity and atrial cardiomyopathy?
This study identifies distinct roles for macrophage subpopulations in atrial adiposity and remodeling, suggesting CCR2+ macrophages as a potential therapeutic target to prevent atrial fibrillation.
Links macrophage recruitment to atrial adiposity in obese mice; hypothesis-generating for inflammation in atrial cardiomyopathy progression.
BACKGROUND: Inflammation is associated with atrial fibrillation, but its precise impact on the long-term progression of the atrial fibrillation substrate, also called atrial cardiomyopathy, remains debated. METHODS AND RESULTS: Here, using spatial gene expression analysis, macrophage subpopulations mainly confined to the epicardial fat tissue were identified in the human atria. In a mouse model of obesity and atrial cardiomyopathy, macrophage recruitment was associated with atrial adiposity. Single-cell RNA sequencing allowed the identification of Lyve1 + -resident and CCR2 + monocyte-derived macrophages in obese mouse atria. In obese mice, depleting Lyve1 + -macrophages prevented early fat expansion and led to myocardial dystrophy, while CCR2 + -macrophage depletion prevented fibro-fatty remodeling, atrial dilation, and atrial fibrillation. CONCLUSIONS: These data highlight the pivotal role of macrophages in atrial adiposity, in particular that of Lyve1 + -macrophages during adipose tissue expansion.
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Crépin et al. (2026) studied Atrial cardiomyopathy and obesity. Macrophage depletion (Lyve1+ and CCR2+) was evaluated on Fibro-fatty remodeling, atrial dilation, and atrial fibrillation. Depleting CCR2+ macrophages in obese mice prevented fibro-fatty remodeling, atrial dilation, and atrial fibrillation, while depleting Lyve1+ macrophages prevented early fat expansion.
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