TGFB1 and myocardial infarction: By contrast, the ability of C21 to reduce fibrosis in persistent reactive fibrotic models of CVD probably reflects both impaired collagen production (decreased TGF-β1 and collagen), as well as increased degradation due to raised MMP levels (Koulis et al., 2015), which is clearly different to abruptly developing MI-induced cardiac remodeling (Figure 1).