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.
Scientific Claim
Cardiomyocyte-specific deletion of hepcidin in mice leads to cardiomyocyte iron deficiency, resulting in fatal cardiac dysfunction with reduced ejection fraction and increased apoptosis, despite normal systemic iron homeostasis.
Original Statement
“We find that while both models maintain normal systemic iron homeostasis, they nonetheless develop fatal contractile and metabolic dysfunction as a consequence of cardiomyocyte iron deficiency.”
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 cardiomyocyte hepcidin deletion and cardiac dysfunction in mice, but cannot establish causation due to lack of randomization and small sample size. 'Leads to' is too strong; 'is associated with' is more appropriate.
More Accurate Statement
“Cardiomyocyte-specific deletion of hepcidin in mice is associated with cardiomyocyte iron deficiency and fatal cardiac dysfunction with reduced ejection fraction and increased apoptosis, despite normal systemic iron homeostasis.”
Evidence from Studies
Supporting (1)
An essential cell-autonomous role for hepcidin in cardiac iron homeostasis