Stabilisation of HIF signalling in the mouse epicardium extends embryonic potential and neonatal heart regeneration.

Can the authors speculate why the difference exists and how this decrease arises? For example, are there decreased pro-inflammatory signals in Phd2 deleted mice? Is there decreased collagen deposition and ECM gene expression? Do macrophage recruitment into the infarct zone differ between mutant/treated vs WT? The representative images in Figure 6k reveal a trend towards reduced fibrosis with Molidistat treatment (Figure 6l), but across all hearts analysed this was not as significant as observed in the epicardial-specific deletion injured hearts (Figure 5g, h).

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