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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

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Larger particles, by contrast, benefit from prolonged circulation and enhanced accumulation at the tumor periphery, but their restricted penetration into deeper tissue regions remains a persistent limitation [33, 38, 40]

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