| First Author | Hulsmans M | Year | 2023 |
| Journal | Science | Volume | 381 |
| Issue | 6654 | Pages | 231-239 |
| PubMed ID | 37440641 | Mgi Jnum | J:338467 |
| Mgi Id | MGI:7512832 | Doi | 10.1126/science.abq3061 |
| Citation | Hulsmans M, et al. (2023) Recruited macrophages elicit atrial fibrillation. Science 381(6654):231-239 |
| abstractText | Atrial fibrillation disrupts contraction of the atria, leading to stroke and heart failure. We deciphered 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 cross-talk 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. |
