September 20, 2025CirculationOpen Access

Fibroblast-Specific Loss of TGF-β Signaling Mediates Lipomatous Metaplasia in the Infarcted Heart

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Fibroblast-specific disruption of TGF-β signaling leads to increased postinfarction cardiac rupture and a matrix-degrading fibroblast phenotype.
Deletion of TbR2 resulted in 30% to 40% replacement of scar tissue with adipocytes, highlighting the role of TGF-β in cardiac injury.
Lineage tracing confirmed that TGF-β signaling disruption drives fibroblast-to-adipocyte conversion through Smad-independent pathways.
In vitro studies demonstrated that TbR2 inhibition triggered adipogenesis-related gene expression in cardiac fibroblasts.

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Research reveals disrupted TGF-β signaling promotes fibroblast-to-adipocyte conversion in the heart, indicating a link to arrhythmogenesis.

Tuleta et al. (2025) studied this question.

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Research reveals disrupted TGF-β signaling promotes fibroblast-to-adipocyte conversion in the heart, indicating a link to arrhythmogenesis.