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.
Scientific Claim
Cardiomyocyte-specific expression of hepcidin-resistant ferroportin in mice produces cardiac dysfunction identical to hepcidin deletion, confirming that hepcidin regulates cardiac iron homeostasis through ferroportin.
Original Statement
“Like Hampfl/fl;Myh6.Cre+ mice, Slc40a1 C326Yfl/fl;Myh6.Cre+ mice also had increased mortality relative to their littermate controls... The similarity between Hampfl/fl;Myh6.Cre+ and Slc40a1 C326Yfl/fl;Myh6.Cre+ mice in terms of the nature and time course of cardiac dysfunction suggests a common mechanism of cardiac dysfunction involving upregulation of cardiomyocyte FPN.”
Evidence Quality Assessment
Claim Status
appropriately stated
Study Design Support
Design supports claim
Appropriate Language Strength
association
Can only show association/correlation
Assessment Explanation
The study shows an association between hepcidin-resistant ferroportin expression and cardiac dysfunction, but cannot establish causation due to study design limitations. 'Produces' is too strong; 'is associated with' is more appropriate.
More Accurate Statement
“Cardiomyocyte-specific expression of hepcidin-resistant ferroportin in mice is associated with cardiac dysfunction identical to hepcidin deletion, confirming that hepcidin regulates cardiac iron homeostasis through ferroportin.”
Evidence from Studies
Supporting (1)
An essential cell-autonomous role for hepcidin in cardiac iron homeostasis