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 mice don't have hepcidin in their heart cells or have a version of ferroportin that can't respond to hepcidin, their heart cells lose too much iron, causing the heart cells to become iron deficient.

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.

When mice lose the ability to make hepcidin in their heart cells, their heart cells don't get enough iron, which causes their hearts to weaken and eventually fail, even though their overall body iron levels are normal.

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

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.