Key result
Ankrd1a loss increases border zone cardiomyocyte dedifferentiation but is dispensable for overall ventricular regeneration.
Why the study?
To gain insight into the expression profile and precise roles of the stress-responsive ankrd1a gene in different cardiac structures at key time points during zebrafish heart regeneration.
The ankrd1a gene serves as a marker and fine-tuner of cardiomyocyte dedifferentiation during zebrafish heart regeneration, though it is dispensable for overall ventricular regeneration.
Caution warranted in targeting ANKRD1 for cardiac regeneration therapies; extends zebrafish dedifferentiation research but leaves mammalian necessity open.
In contrast to humans, zebrafish have an outstanding ability to regenerate injured heart through a highly orchestrated process involving all cardiac structures. To replace the lost myocardium, resident cardiomyocytes (CMs) dedifferentiate and proliferate, invading the injured area. The response of the myocardium is preceded by the activation of the epicardium and endocardium, which form active scaffolds to provide mechanical and paracrine support to guide regeneration. New CMs use protrusions to migrate and invade fibrotic injured tissue, replacing it with functional myocardium. Here, we investigated the expression profile of the stress-responsive ankrd1a gene in different cardiac structures, at key time points during regeneration, aiming to gain insight into its precise roles during zebrafish heart regeneration. In the TgBAC(ankrd1a:EGFP) reporter line, transgene upregulation was restricted to the myocardium, initiated as early as 15 h post-cryoinjury, and consistently marked CMs bordering the injury or scar area during regeneration. Transcriptome profiling and immunostaining revealed a potential role of ankrd1a in regulating CMs' dedifferentiation, as well as changes in the expression of genes associated with antigen presentation and extracellular matrix composition in the ankrd1a mutant. Our results indicate that ankrd1a is dispensable for ventricular regeneration after cryoinjury, while it may serve as a marker and fine-tuner in the healing process of injured cardiac muscle. • ankrd1a is upregulated in cardiomyocytes lining the injury or scar during zebrafish heart regeneration. • ankrd1a :EGFP reporter upregulation occurs early after cryoinjury and remains restricted to the myocardium. • Loss of ankrd1a function increases number of dedifferentiating cardiomyocytes in the border zone. • ankrd1a serves as a marker and fine-tuner of the zebrafish heart regeneration response.
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Boskovic et al. (2026) studied Zebrafish heart regeneration after cryoinjury. ankrd1a loss of function was evaluated on Ventricular regeneration and cardiomyocyte dedifferentiation. Loss of ankrd1a function increases the number of dedifferentiating cardiomyocytes in the border zone, though it is dispensable for overall ventricular regeneration after cryoinjury.
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