Fig. 2.

Potential role of LRG1 in cardiac remodelling. In the failing heart, the ability of blood vessels to respond to angiogenic factors is compromised, fibroblasts acquire myofibroblast phenotype by expressing increased ECM protein, and cardiomycytes are enlarged and undergo increased apoptosis. TGFβ1 mainly signals through ALK5 in ECs, cardiomyocyte and myofibroblasts leading to cardiac remodelling. In LRG1-treated heart, LRG1 switches TGFβ1 signalling towards the proangiogenic ALK1 signalling in ECs and promotes blood vessel formation. In myofibroblasts, LRG1 competes with TGFβ to bind ALK5 and antagonise TGFβ-induced ECM synthesis and to prevent fibrosis. With the presence of LRG1, there is reduced cardiomyocyte apoptosis and size