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These findings suggest that GPX4 overexpression leads to ferroptosis deficiency in HK-2 cells and that the progression of TGF--induced fibrosis might be regulated by ferroptosis through the TGF-/Smad signaling pathway and related profibrotic cytokines

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47, 48, 49 This study provides evidence that GSH deficits are also present in patients with BP, indicating that the reduction of peripheral GSH is a common molecular signature of SZ and BP

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