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Although the physiological role of ferroptosis remains unclear, it can be triggered by pharmacological disruption of cellular lipid peroxidation repair or by oxidative stress associated with degeneration

These disruptions are associated with disease subtypes, progression rates, and clinical outcomes (334, 335, 338354, 358), and studies have shown that iron chelation therapy can delay motor neuron degeneration and extend survival in ALS mouse models (352, 355, 358) ( Figure 8 )

These results suggest that increased tumor burden in the absence of host SPARC is a consequence of reduced collagen deposition, a disrupted vascular basement membrane, enhanced vascular function and an immune-tolerant, pro-metastatic microenvironment

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