Heart cells make and release hepcidin using a process that requires the enzyme Furin, and they release more of it when the body is low on iron.

Scientific Claim

Cardiac hepcidin is secreted by cardiomyocytes in a Furin-dependent manner, and its secretion increases during iron deficiency.

Original Statement

“When we measured HAMP in supernatants of cardiomyocytes treated with the Furin inhibitor decanoyl-Arg-Val-Lys-Arg-chloromethylketone (CMK), we found no increase in HAMP release following DFO treatment... Furin expression was upregulated in the hearts of mice provided an iron-deficient diet and in cardiomyocytes treated with DFO.”

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 Furin inhibition and reduced hepcidin secretion, and between iron deficiency and increased hepcidin secretion, but cannot establish causation due to study design limitations. 'Is secreted' and 'increases' are appropriate as they describe observed associations.

More Accurate Statement

“Cardiac hepcidin is associated with secretion by cardiomyocytes in a Furin-dependent manner, and its secretion is associated with increase during 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 the body is low on iron, the heart makes more hepcidin, which might help protect the heart from damage during iron deficiency.

84%

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.

80%

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.

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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.

79%

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.

76%