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Although ACSL4 is consistently upregulated in OA cartilage and linked to ferroptosis progression, its inhibition must be balanced to avoid disrupting normal PUFA metabolism required for membrane integrity and repair ( Altogether, these examples underscore that despite encouraging experimental results, ferroptosis-targeted drugs face multiple translational bottlenecks, including systemic toxicity, insufficient targeting, metabolic compensation, and biological heterogeneity

This proposition was based on the higher GSH content found in cell lysate than the medium and was supported initially from the findings of Fernandes and Steele [18] who reported synthesis of GSH by Lc

Humanin: a possible linkage between Alzheimers disease and type 2 diabetes

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Furthermore, studies on LRRK2 deficient mice showed no significant differences in animal behavior compared to the control using the open field test (Hinkle et al., 2012