The ultimate goal in heart failure treatment is to stimulate the heart’s natural regenerative capacity and replace damaged tissue. Previous work has shown that lower vertebrates such as zebrafish can efficiently regenerate cardiac cells after injury. However, current methods to induce injury in an experimental setting are invasive, making it difficult to assess the maximum regenerative potential of cardiomyocytes. Wang et al. minimised this problem by creating a zebrafish model in which cardiomyocytes could be inducibly depleted. The authors used a tamoxifen-inducible promoter to drive expression of cytotoxic diphtheria toxin A (DTA) specifically in cardiomyocytes. On exposure to tamoxifen, death of a high proportion of cardiomyocytes resulted in cardiac failure. After several days, ablated cardiomyocytes fully regenerated from highly proliferative neighbouring cardiomyocytes that had not been ablated, replacing the structure and function of the damaged tissue. This model system should provide new insight into heart-regenerative mechanisms.
- Written by editorial staff. © 2011. Published by The Company of Biologists Ltd.
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