Fibroblast-Specific Loss of TGF-β Signaling Mediates Lipomatous Metaplasia in the Infarcted Heart
Authors' conclusion
TGF-β signaling plays a central role in maintaining fibroblast cell specification after cardiac injury. Fibroblast-to-adipocyte conversion induced by disrupted TGF-β signaling may underlie scar-associated lipomatous metaplasia and may play an important role in the pathogenesis of heart failure and arrhythmogenesis in patients with ischemic cardiomyopathy.
Study context
- Population
- Mice undergoing reperfused and nonreperfused MI; human infarcted hearts (single-cell RNA sequencing)
- Comparison
- Fibroblast-specific TbR2 loss vs controls
- Outcome
- Postinfarction cardiac rupture, adipocyte replacement of mature scar and fibroblast-to-adipocyte conversion with fibroblast-specific TbR2 loss
Methodological detailsmouse models, lineage tracing, human single-cell RNA sequencing
- Mouse models
- Lineage tracing
- Human single-cell RNA sequencing
Main finding
As reported in the abstract
Fibroblast-specific TbR2 loss: replacement of mature scar with adipocytes in reperfused and nonreperfused infarcts
30% to 40%
Original publication
Fibroblast-Specific Loss of TGF-β Signaling Mediates Lipomatous Metaplasia in the Infarcted Heart. Circulation. Published 19 September 2025. doi:10.
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