Sulf1 regulates inflammation via modulation of TGF-β dependent epicardial activation.

Sulf1 modulates TGF-β-dependent epicardial activation and inflammation, with its disruption causing regeneration defects and increased fibrosis in zebrafish hearts.

• Why it matters: Understanding how epicardial activation influences immune responses is crucial for advancing heart regeneration strategies, as the mechanisms linking epicardial signals to inflammation remain largely unknown.
• What they did: The study used gain- and loss-of-function tools to show that Sulf1 upregulation after injury regulates epicardial activation and regeneration via TGF-β signaling, with scRNA-seq revealing effects on macrophage recruitment.
• The result: Disruption of sulf1 impairs cardiomyocyte regeneration, increases fibrosis, and stimulates inflammation, while overexpression of sulf1 reverses these effects, highlighting Sulf1’s role in modulating inflammation during heart regeneration.