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Collectively, our study identifies the L2HGDH-L2HG axis as a previously unrecognized metabolic checkpoint controlling ferroptosis sensitivity in liver cancer and uncovers glutathione degradation as a therapeutically exploitable vulnerability for ferroptosis-based treatment strategies in HCC.

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It supports tissue repair, inflammation modulation, and regenerative signaling across muscles, tendons, ligaments, and the gut lining, making it a focus for research in angiogenesis research, injury tissue remodelling, and wellness

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