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Oxford

£17,472

2015

The epicardium, which orchestrates coronary vessel development, is partially reactivated post-myocardial infarction to facilitate neovascularisation and regeneration. However, a key limitation to the efficiency of epicardium-based repair is the low proportion of cells that undergo epithelial-mesenchymal transition (EMT) to contribute to the pool of active progenitors at the infarct site. We identified sulfatases as enzymes that control the sensitivity of epicardial cells to the growth factors that drive EMT. The CRM pump priming award enabled the generation of global and conditional knockout lines, which are now being used to validate sulfatases as key regulators of EMT and putative targets to therapeutically enhance EMT and advance epicardium-based regenerative strategies.

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