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730 FtMt protein expression is significantly upregulated in MCAO/R mice, and the absence of FtMt promotes free iron deposition and lipid peroxidation, which aggravates ferroptosis and brain injury caused by MCAO/R

Our hypothesis calls for precision nutrition models that stratify patients based on biochemical profiles and sex-specific responsesgenerating new paradigms for thyroid-CVD comanagement [9]

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