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.

Scientific Claim

Cardiomyocyte iron efflux is increased in mice with cardiomyocyte-specific hepcidin deletion or hepcidin-resistant ferroportin, leading to cardiomyocyte iron deficiency.

Original Statement

“Iron Fe55 efflux was indeed significantly greater in cardiomyocytes isolated from Hampfl/fl;Myh6.Cre+ and Slc40a1 C326Yfl/fl;Myh6.Cre+ hearts than in cardiomyocytes isolated from their respective controls... the iron content of the cardiomyocyte fraction was significantly lower in Hampfl/fl;Myh6.Cre+ and in Slc40a1 C326Yfl/fl;Myh6.Cre+ mice than in their respective controls.”

From study:An essential cell-autonomous role for hepcidin in cardiac iron homeostasis

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 deletion/resistance and increased iron efflux, but cannot establish causation due to study design limitations. 'Leads to' is too strong; 'is associated with' is more appropriate.

More Accurate Statement

“Cardiomyocyte iron efflux is associated with increased in mice with cardiomyocyte-specific hepcidin deletion or hepcidin-resistant ferroportin, leading to cardiomyocyte iron deficiency.”

Evidence from Studies

Supporting (1)

An essential cell-autonomous role for hepcidin in cardiac iron homeostasis

Randomized Controlled Trial

Animal

2016 Nov 29

Contradicting (0)

No contradicting evidence found

Source Study

An essential cell-autonomous role for hepcidin in cardiac iron homeostasis

Score: 11

DOI: 10.7554/elife.19804

Similar Assertions

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.

87%

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.

85%

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.

82%

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

77%

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.

76%