In the heart, the way hepcidin responds to iron levels is different from how it works in the liver - when the body is low on iron, the heart makes more hepcidin protein even though the gene for it is less active.

When the body is low on iron, the heart makes more hepcidin, which might help protect the heart from damage during iron deficiency.

Giving iron directly into the bloodstream of mice with heart cell hepcidin deficiency stops their hearts from failing, proving that the heart problems are caused by the heart cells not getting enough iron.

Heart cells make and release hepcidin using a process that requires the enzyme Furin, and they release more of it when the body is low on iron.

When mice have heart cells that can't respond to hepcidin (because they have a special version of ferroportin), their hearts fail in the same way as when they don't have hepcidin at all, showing that hepcidin works by controlling ferroportin in heart cells.

When female mice can't make a protein called hepcidin, they end up with too much iron in their blood and body, and their red blood cell numbers go up — this suggests hepcidin normally keeps iron levels in check.