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Updated: May 7, 2026
07:25
Isolation of Macrophage Subsets and Stromal Cells from Human and Mouse Myocardial Specimens
Published on: December 17, 2019
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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
Summary
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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