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It was found that GCH1 overexpression selectively protected phosphatidylcholines with two PUFA tails from oxidative degradation, and these phospholipids drove ferroptosis, thereby protecting cells from ferroptosis
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This oxidative damage severely impairs the mitochondria's ability to produce adenosine triphosphate (ATP), the currency of cellular energy
Thyroid: Off J Am Thyroid Assoc (2003) 13(3):26571
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