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
The heart makes its own iron regulator called hepcidin to control iron levels inside heart cells. Without it, heart cells lose too much iron and stop working properly.
No biological mechanisms were identified in this study. This may be an epidemiological, observational, or survey-based study that reports associations rather than proposing causal biological pathways.
Systematic Reviews & Meta-Analyses
Max 100Randomized Controlled Trials
Max 90Cohort Studies
Max 72Case-Control Studies
Max 58Cross-Sectional Studies
Max 44Case Reports & Case Series
Max 30Expert Opinion & Narrative Reviews
Max 511 / 90
Evidence Score
Participants are randomly assigned to treatment or control groups, minimizing bias. Considered the gold standard for testing whether an intervention causes an effect.
Not medical advice. For informational purposes only. Always consult a healthcare professional. Terms
The heart makes its own iron regulator called hepcidin to control iron levels inside heart cells. Without it, heart cells lose too much iron and stop working properly.
No biological mechanisms were identified in this study. This may be an epidemiological, observational, or survey-based study that reports associations rather than proposing causal biological pathways.
Systematic Reviews & Meta-Analyses
Max 100Randomized Controlled Trials
Max 90Cohort Studies
Max 72Case-Control Studies
Max 58Cross-Sectional Studies
Max 44Case Reports & Case Series
Max 30Expert Opinion & Narrative Reviews
Max 511 / 90
Evidence Score
Participants are randomly assigned to treatment or control groups, minimizing bias. Considered the gold standard for testing whether an intervention causes an effect.
Publication
Authors
Lakhal-Littleton S, Wolna M, Chung YJ, Christian HC, Heather LC, Brescia M, Ball V, Diaz R, Santos A, Biggs D, Clarke K, Davies B, Robbins PA
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.