When mice lose hepcidin only in their heart cells, their overall body iron levels and storage remain normal, showing that heart hepcidin doesn't affect the body's overall iron balance.

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-specific hepcidin deletion and normal systemic iron markers, but cannot establish causation due to study design limitations. 'Does not affect' is too strong; 'is not associated with affecting' is more appropriate.

More Accurate Statement

“Cardiomyocyte-specific hepcidin deletion is associated with normal systemic iron homeostasis, as evidenced by normal liver iron stores and circulating iron markers.”

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 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.

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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.

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In the heart, the way hepcidin responds to iron levels is different from how it works in the liver - when the body is low on iron, the heart makes more hepcidin protein even though the gene for it is less active.

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

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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.

73%