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Abstract Atrial fibrillation (AFib) and the risk of its lethal complications are propelled by fibrosis, which induces electrical heterogeneity and gives rise to reentry circuits. Atrial TREM2 + macrophages secrete osteopontin (encoded by Spp1 ), a matricellular signaling protein that engenders fibrosis and AFib. Here we show that silencing Spp1 in TREM2 + cardiac macrophages with an antibody-siRNA conjugate reduces atrial fibrosis and suppresses AFib in mice, thus offering a new immunotherapy for the most common arrhythmia.
Published April 23 within past 14 days; rapid uptake with >300 downloads in first week, active discussion on X and ResearchGate among electrophysiologists (estimated 150+ mentions), novel macrophage target generating mechanistic excitement.
Momin et al. (Sat,) studied this question.