What is it about?

Ferroptosis is a clinically important failsafe event that contributes to cell death in diseases such as Alzheimer’s disease, stroke, myocardial infarction, and acute kidney injury. A physiological role of ferroptosis, however, has not been identified. Here, we show that fish viruses can express an insulin-like peptide that functions as a potent inhibitor of ferroptosis, indicating that virally infected cells evade ferroptosis in lower organisms. The antiferroptotic properties of the molecule, which we refer to as viral peptide inhibitor of ferroptosis-1 (vPIF-1), require a functional region that is known as the C-peptide. This report identifies a virally encoded protein that inhibits ferroptosis.

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Why is it important?

It is still not known why we conserve a ferroptosis program in our genome. Our data indicate that ferroptosis is a helpful anti-viral defense mechanism. Other forms of cell death, such as apoptosis or necroptosis, are known to kill virally infected cells.


We develop pharmacological inhibitiors of ferroptosis to treat acute settings like heart attacks, strokes and acute kidney injury, but also in the long run to inhibit neurodegeneration. We cannot exclude that inhibition of ferroptosis long term might support viral infections.

Andreas Linkermann
Technical University Dresden

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This page is a summary of: vPIF-1 is an insulin-like antiferroptotic viral peptide, Proceedings of the National Academy of Sciences, May 2023, Proceedings of the National Academy of Sciences,
DOI: 10.1073/pnas.2300320120.
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