Results We demonstrated that the adult heart reverts to a hypertrabeculated state between 1 and 5 days post-MI and repeats the process of endocardial compaction from 7-14 days. This process appears to facilitate endocardium-derived neovascularization, leading to formation of mature sub-endocardial vessels after infarction. We observed reactivation of the Notch pathway in the endocardium following MI, in keeping with its role as a key regulator of these processes in development. Using a Notch1

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... ss-of-function mouse model targeted by an endothelial-specific Cre, we observed impaired trabeculation with reduced sub-endocardial vessel count after disruption of Notch activity. (Figure 1 ) Conclusion We established that de novo vessel formation constitutes a significant component of the neovascular response and revealed that the endocardium is a major contributory source. Notch1 was identified as a key driver in this remodelling process and, moreover, our data suggest a role for Notch in driving endothelial-mesenchymal transition (EndMT) to provide smooth muscle support to newly formed vessels. Ongoing work seeks to determine whether targeting trabeculation in the adult heart will contribute to improved neovascularisation post-MI.