Why the study?
Does ablation of CCR2 improve LV hypertrophy, cardiac fibrosis, or diastolic dysfunction in a mouse model of early HFpEF?
Does ablation of CCR2 improve LV hypertrophy, cardiac fibrosis, or diastolic dysfunction in a mouse model of early HFpEF?
In a mouse model of early HFpEF, CCR2 ablation improves LV hypertrophy but not fibrosis or diastolic dysfunction, indicating that anti-inflammatory therapies alone may be insufficient without antifibrotic treatment.
May inform CCR2-targeted anti-inflammatory strategies for hypertrophy in early HFpEF; leaves open combined antifibrotic approaches for diastolic dysfunction.
Development of a multi-comorbidity model induces early heart failure with preserved ejection fraction (HFpEF) in male mice. Early HFpEF is marked by circulating proinflammatory monocytosis (Ly6C hi ) and a disruption in the balance between monocyte-derived macrophage infiltration (CCR2 + ) and resident macrophages (TIMD4 + ). Ablation of CCR2, which prevents recruitment of classical macrophages, improves left ventricle (LV) hypertrophy in early HFpEF but not cardiac fibrosis or diastolic dysfunction. Anti-inflammatory therapies alone, without antifibrotic treatment, will likely not prevent the development of HFpEF.
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Raman et al. (2025) studied this question.
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