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Taken together, the observed lipidome changes suggest that C32E8.9 plays a crucial role in regulating fatty acid elongation and saturation, and mediating lipidomic changes taking place under mitochondrial translation inhibition

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Although preclinical models suggest that DFX may reduce white matter injury and perihematomal edema, meta-analyses have reported inconsistent effects on neurological recovery.129,130 Several barriers hinder clinical application: (1) limited BBB penetration restricts effective intracerebral drug delivery;131 (2) chronic toxicity, including auditory, retinal, and hematological adverse effects, limit long-term use;132 (3) short plasma half-lives of agents like LIP1 and DFX necessitate frequent dosing;123,133 (4) narrow therapeutic focus on lipid peroxidation fails to address broader iron imbalance and GPX4 dysfunction;134 (5) low oral bioavailability and dose-related central nervous system depression reduce effectiveness;;133,135 (6) drug interactions, particularly with immunosuppressants, heighten bleeding and infection risks;133,136 and (7) natural chelators often lack validated safety and efficacy data, despite encouraging preclinical data.137 To improve treatment efficacy, ferroptosis-targeted therapies must shift from single-target agents to integrated, multi-pathway strategies