Figure 5.

Schematic diagram outlining the proposed signalling pathways by which IMD might influence (a) contraction; (b) hypertrophic remodelling; (c) protection against the deleterious consequences of oxidative stress directly in ventricular cardiomyocytes. Adenylate cyclase (AC); protein kinase A (PKA); protein kinase C (PKC); diacylglycerol (DAG); mitogen-activated protein kinase (MAPK); receptor tyrosine kinase (rTK); phospholipase C-β (PLC-β); extracellular signal-regulated kinase (ERK); phosphoinositide 3-kinase (PI3K); receptor component protein (RCP). IMD, intermedin.