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Recruited macrophages elicit atrial fibrillation

Maarten Hulsmans1,2, Maximilian J Schloss1,2, I-Hsiu Lee1,2

  • 1Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.

Science (New York, N.Y.)
|July 13, 2023
PubMed

Insights

Immune cells, specifically SPP1+ macrophages, drive atrial fibrillation by disrupting heart contractions. Targeting these macrophages offers a new therapeutic strategy for preventing stroke and heart failure.

Area of Science:

  • Cardiovascular Research
  • Immunology
  • Cell Biology

Background:

  • Atrial fibrillation (AF) impairs atrial contraction, increasing risks of stroke and heart failure.
  • The roles of immune and stromal cells in AF pathogenesis remain incompletely understood.

Purpose of the Study:

  • To investigate the contribution of immune and stromal cells to atrial fibrillation.
  • To identify specific cellular players and molecular mechanisms driving AF.

Main Methods:

  • Single-cell RNA sequencing of human and mouse atria.
  • Development of a mouse model combining hypertension, obesity, and mitral valve regurgitation (HOMER).
  • Genetic manipulation (Ccr2 knockout, Spp1 deletion) and cell-cell interaction analysis.

Main Results:

  • Single-cell transcriptomics revealed expansion of inflammatory monocytes and SPP1+ macrophages in human and HOMER mouse atria.
  • HOMER mice exhibited enlarged, fibrotic, and AF-prone atria, mirroring human pathology.
  • Inhibiting monocyte migration (Ccr2-/-) and deleting Spp1 reduced AF incidence in HOMER mice.
  • SPP1 was identified as a key signaling molecule mediating cross-talk between immune and stromal cells, promoting AF.

Conclusions:

  • SPP1+ macrophages are key drivers of atrial fibrillation.
  • Targeting SPP1+ macrophages represents a potential immunotherapeutic strategy for AF.
  • Understanding immune-stromal cell interactions is crucial for developing novel AF treatments.

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