Key result
Apex resection in neonatal mice did not result in complete regeneration, with damaged hearts being 9.8% shorter and weighing 14% less than sham controls, alongside massive fibrotic scarring.
Neonatal mouse hearts do not completely regenerate following apex resection, questioning the utility of this model for studying adult cardiac regeneration.
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Questions neonatal apex resection model utility for adult regeneration research; leaves open need for validated alternatives.
The mammalian heart has generally been considered nonregenerative, but recent progress suggests that neonatal mouse hearts have a genuine capacity to regenerate following apex resection (AR). However, in this study, we performed AR or sham surgery on 400 neonatal mice from inbred and outbred strains and found no evidence of complete regeneration. Ideally, new functional cardiomyocytes, endothelial cells, and vascular smooth muscle cells should be formed in the necrotic area of the damaged heart. Here, damaged hearts were 9.8% shorter and weighed 14% less than sham controls. In addition, the resection border contained a massive fibrotic scar mainly composed of nonmyocytes and collagen disposition. Furthermore, there was a substantial reduction in the number of proliferating cardiomyocytes in AR hearts. Our results thus question the usefulness of the AR model for identifying molecular mechanisms underlying regeneration of the adult heart after damage.
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Andersen et al. (2014) studied Heart damage/regeneration (n=400). Apex resection (AR) vs. Sham surgery was evaluated on Complete regeneration (heart length, weight, fibrotic scar, proliferating cardiomyocytes). Apex resection in neonatal mice did not result in complete regeneration, with damaged hearts being 9.8% shorter and weighing 14% less than sham controls, alongside massive fibrotic scarring.
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