Originally identified in human plasma, this peptidecopper complex functions as a biological repair signal that supports healthier cellular activity patterns
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In FXS, CGG repeat expansions in the FMR1 gene lead to the loss of FMRP, impairing the translation of GABAA receptor mRNAs, particularly the GABAA 5 subunit, reducing receptor density in the amygdala and nucleus accumbens, resulting in delayed language development and autistic-like behaviors (138)
The specific mechanisms by which ferroptosis contributes to CHD pathophysiology require further elucidation, particularly regarding its interrelationship with other cell death pathways (e.g., apoptosis, necrosis)
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