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Lee, I-Hsiu

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Lee

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I-Hsiu

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Lee, I-Hsiu

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    Recruited macrophages elicit atrial fibrillation
    Hulsmans, Maarten; Schloss, Maximilian J.; Lee, I-Hsiu; Bapat, Aneesh; Iwamoto, Yoshiko; Vinegoni, Claudio; Paccalet, Alexandre; Yamazoe, Masahiro; Grune, Jana; Pabel, Steffen; Momin, Noor; Seung, Hana; Kumowski, Nina; Pulous, Fadi; Keller, Daniel; Bening, Constanze; Green, Ursula; Lennerz, Jochen K.; Mitchell, Richard N.; Lewis, Andrew; Casadei, Barbara; Iborra-Egea, Oriol; Bayes-Genis, Antoni; Sossalla, Samuel; Ong, Chin Siang; Pierson, Richard N.; Aster, Jon C.; Rohde, David; Wojtkiewicz, Gregory R.; Weissleder, Ralph; Swirski, Filip K.; Tellides, George; Tolis, George; Melnitchouk, Serguei; Milan, David J.; Ellinor, Patrick T.; Naxerova, Kamila; Nahrendorf, Matthias
    Atrial fibrillation disrupts contraction of the atria, leading to stroke and heart failure. We here decipher how immune and stromal cells contribute to atrial fibrillation. Single-cell transcriptomes from human atria documented inflammatory monocyte and SPP1+ macrophage expansion in atrial fibrillation. Combining hypertension, obesity and mitral valve regurgitation (HOMER) in mice elicited enlarged, fibrosed, and fibrillation-prone atria. Single-cell transcriptomes from HOMER mouse atria recapitulated cell composition and transcriptome changes observed in patients. Inhibiting monocyte migration reduced arrhythmia in Ccr2−∕− HOMER mice. Cell–cell interaction analysis identified SPP1 as a pleiotropic signal that promotes atrial fibrillation through crosstalk with local immune and stromal cells. Deleting Spp1 reduced atrial fibrillation in HOMER mice. These results identify SPP1+ macrophages as targets for immunotherapy in atrial fibrillation.