Mechanism characteristic of Type 1 iron-deficient heart failure. The delivery of circulating iron is prioritized to erythroblasts in the bone marrow. When transferrin saturations are low (due to either absolute or functional iron deficiency), iron is released for utilization by other organs (i.e. the heart), even though such release impairs erythropoiesis, leading to anaemia. Cardiomyocytes upregulate the entry of iron and suppress the egress of iron (and iron is also released from the ferritin nanocage); these actions support cytosolic iron levels within the heart. Given the relationship between iron in the circulation and in cardiomyocytes, the measurement of transferrin saturation represents a reasonable metric to identify patients most likely to experience a reduced risk of major heart failure events in large-scale trials