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I went into this treatment as a hopeful skeptic and now I regret I didnt start it earlier

The rationale is mechanistic: the two compounds operate through distinct but non-overlapping pathways, with tissue targets that complement rather than duplicate each other

That's the real reason this molecule gets so much attention

reported that ACSL4 played a critical role in ferroptosis-mediated tissue injury in IR mouse model, and special protein 1 could increase ACSL4 transcription and further promote the progression of ferroptosis (Li et al., 2019a)

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