Heart's own iron regulator
An essential cell-autonomous role for hepcidin in cardiac iron homeostasis
Not medical advice. For informational purposes only. Always consult a healthcare professional. Terms
Surprising Findings
Cardiac hepcidin increases during systemic iron deficiency while its gene expression decreases
This is the opposite of how liver hepcidin works—liver hepcidin increases when iron is high, but heart hepcidin increases when iron is low, suggesting a protective role for the heart.
Practical Takeaways
Heart failure patients with normal hemoglobin but fatigue might benefit from checking cardiac-specific iron levels.
Not medical advice. For informational purposes only. Always consult a healthcare professional. Terms
Surprising Findings
Cardiac hepcidin increases during systemic iron deficiency while its gene expression decreases
This is the opposite of how liver hepcidin works—liver hepcidin increases when iron is high, but heart hepcidin increases when iron is low, suggesting a protective role for the heart.
Practical Takeaways
Heart failure patients with normal hemoglobin but fatigue might benefit from checking cardiac-specific iron levels.
Publication
Journal
eLife
Year
2016
Authors
S. Lakhal-Littleton, Magda Wolna, Y. Chung, H. Christian, L. Heather, Marcella Brescia, V. Ball, R. Diaz, A. Santos, D. Biggs, K. Clarke, B. Davies, P. Robbins
Related Content
Claims (10)
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.
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 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.
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 heart cells don't have enough iron, their energy production systems break down, causing mitochondria to malfunction and forcing the cells to rely more on sugar for energy, which happens before the heart starts failing.