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Animal models attempting to replicate the dopaminergic pathology and clinical features of PD have been critical to our understanding of the pathogenic mechanisms of the disease

The previous studies provide strong evidence that iron accumulation is closely involved in the pathological process of secondary injury of TBI, and maintaining iron homeostasis is an effective means against ferroptosis triggered by TBI [49]

Previous studies show that this phenotype switch is mainly related to the metabolic reprogramming per se (11, 12)