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While failure of these compensatory mechanisms could ultimately cause ferroptotic cell death, more subtle changes in intracellular redox balance could also enhance signaling pathways, including those associated with T2 inflammation (10)

So by increasing carnitine levels, the rate of fatty acid oxidation could have been returned to normal levels

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But this short half-life doesn't tell the full story - the peptide triggers cellular processes (collagen synthesis, wound healing, anti-inflammatory cascades) that continue for days after the peptide itself has cleared

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