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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 E; 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.
Afiliação
  • Hulsmans M; Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.
  • Schloss MJ; Department of Radiology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.
  • Lee IH; Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.
  • Bapat A; Department of Radiology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.
  • Iwamoto Y; Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.
  • Vinegoni C; Department of Radiology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.
  • Paccalet A; Cardiovascular Research Center, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.
  • Yamazoe M; Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.
  • Grune J; Department of Radiology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.
  • Pabel S; Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.
  • Momin N; Department of Radiology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.
  • Seung H; Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.
  • Kumowski N; Department of Radiology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.
  • Pulous FE; Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.
  • Keller D; Department of Radiology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.
  • Bening C; Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.
  • Green U; Department of Radiology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.
  • Lennerz JK; Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.
  • Mitchell RN; Department of Radiology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.
  • Lewis A; Department of Internal Medicine II, University Medical Center Regensburg, Regensburg, Germany.
  • Casadei B; Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.
  • Iborra-Egea O; Department of Radiology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.
  • Bayes-Genis A; Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.
  • Sossalla S; Department of Radiology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.
  • Ong CS; Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.
  • Pierson RN; Department of Radiology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.
  • Aster JC; Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.
  • Rohde D; Department of Radiology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.
  • Wojtkiewicz GR; Department of Thoracic and Cardiovascular Surgery, University Hospital Wuerzburg, Wuerzburg, Germany.
  • Weissleder R; Department of Thoracic and Cardiovascular Surgery, University Hospital Wuerzburg, Wuerzburg, Germany.
  • Swirski FK; Department of Pathology, Center for Integrated Diagnostics, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.
  • Tellides G; Department of Pathology, Center for Integrated Diagnostics, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.
  • Tolis G; Department of Pathology, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.
  • Melnitchouk S; Radcliffe Department of Medicine, NIHR Biomedical Research Centre, University of Oxford, Oxford, UK.
  • Milan DJ; British Heart Foundation Centre of Research Excellence, University of Oxford, Oxford, UK.
  • Ellinor PT; Radcliffe Department of Medicine, NIHR Biomedical Research Centre, University of Oxford, Oxford, UK.
  • Naxerova K; British Heart Foundation Centre of Research Excellence, University of Oxford, Oxford, UK.
  • Nahrendorf M; Institut del Cor Germans Trias i Pujol, CIBERCV, Badalona, Barcelona, Spain.
Science ; 381(6654): 231-239, 2023 07 14.
Article em En | MEDLINE | ID: mdl-37440641
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 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.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Fibrilação Atrial / Osteopontina / Macrófagos Limite: Animals / Humans Idioma: En Revista: Science Ano de publicação: 2023 Tipo de documento: Article País de afiliação: Estados Unidos
Texto completo
Imprimir
XML
PubMed Links
Buscar no Google

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Fibrilação Atrial / Osteopontina / Macrófagos Limite: Animals / Humans Idioma: En Revista: Science Ano de publicação: 2023 Tipo de documento: Article País de afiliação: Estados Unidos