Key result
Prrx1b is required for scar-free regeneration of the zebrafish heart, as its loss results in excessive fibrosis and impaired cardiomyocyte proliferation.
Why the study?
The mechanisms that drive permanent scarring versus scar-free regeneration following cardiac injury are not well understood.
Does Prrx1b regulate fibrosis and cardiomyocyte proliferation during heart regeneration?
Population
Zebrafish and human fetal epicardial-derived cells
Comparison
Loss of Prrx1b or Prrx1 manipulation vs controls
Design
In vivo and in vitro experimental study
Authors
Loading...
Prrx1b modulation merits testing in mammalian models; leaves open translation to human cardiac repair.
Does Prrx1b regulate fibrosis and cardiomyocyte proliferation during heart regeneration?
Prrx1b is a key transcription factor that balances fibrosis and regeneration in the injured zebrafish heart by restricting TGFβ and promoting Nrg1-dependent cardiomyocyte proliferation.
Bakker et al. (2021) studied Cardiac injury. Prrx1b was evaluated on Fibrosis and cardiomyocyte proliferation. Prrx1b is required for scar-free regeneration of the zebrafish heart, as its loss results in excessive fibrosis and impaired cardiomyocyte proliferation.
Synapse has enriched 3 closely related papers on similar clinical questions. Consider them for comparative context: