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⁺, and superoxide dismutase (SOD) activity were measured by assay kits to evaluate miR-19b-3p's effect on ferroptosis. In 1-methyl-4-phenylpyridinium (MPP⁺)-treated cells and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated mice, miR-19b-3p was downregulated. Luciferase assays supported ACSL4 as a direct target of miR-19b-3p. Overexpression of miR-19b-3p attenuated ferroptosis-related changes, MPP⁺-induced cell damage, and MPTP-induced motor deficits, whereas ACSL4 overexpression partially reversed these effects. These findings support a role for the miR-19b-3p/ACSL4 axis in regulating ferroptosis-related responses in MPP⁺- and MPTP-based experimental models.
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Wang et al. (2026) studied this question.
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