Hulsmans, Maarten and Schloss, Maximilian J. and Lee, I-Hsiu and Bapat, Aneesh and Iwamoto, Yoshiko and Vinegoni, Claudio and Paccalet, Alexandre and Yamazoe, Masahiro and Grune, Jana and Pabel, Steffen and Momin, Noor and Seung, Hana and Kumowski, Nina and Pulous, Fadi E. and Keller, Daniel and Bening, Constanze and Green, Ursula and Lennerz, Jochen K. and Mitchell, Richard N. and Lewis, Andrew and Casadei, Barbara and Iborra-Egea, Oriol and Bayes-Genis, Antoni and Sossalla, Samuel and Ong, Chin Siang and Pierson, Richard N. and Aster, Jon C. and Rohde, David and Wojtkiewicz, Gregory R. and Weissleder, Ralph and Swirski, Filip K. and Tellides, George and Tolis, George and Melnitchouk, Serguei and Milan, David J. and Ellinor, Patrick T. and Naxerova, Kamila and Nahrendorf, Matthias (2023) Recruited macrophages elicit atrial fibrillation. SCIENCE, 381 (6654). pp. 231-238. ISSN 0036-8075, 1095-9203
Full text not available from this repository. (Request a copy)Abstract
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 Ccr(2-/-) 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.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | ANGIOTENSIN-II; CARDIAC MACROPHAGES; OSTEOPONTIN; FIBROSIS; EXPRESSION; ATHEROSCLEROSIS; INFLAMMATION; ACTIVATION; MECHANISMS; CELLS; |
| Subjects: | 600 Technology > 610 Medical sciences Medicine |
| Divisions: | Medicine > Lehrstuhl für Innere Medizin II |
| Depositing User: | Dr. Gernot Deinzer |
| Date Deposited: | 18 Apr 2024 14:10 |
| Last Modified: | 18 Apr 2024 14:10 |
| URI: | https://pred.uni-regensburg.de/id/eprint/60869 |
Actions (login required)
 |
View Item |
