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Manipulating Ca 2+ homeostasis offers a compelling strategy to balance cellular lipids and cell survival in ferroptosis-associated diseases

The molecular mechanism by which the PfK13 mutations confer artemisinin resistance in clinical isolates may involve multiple cellular and metabolic processes, including hemoglobin uptake and digestion, the unfolded protein stress response, mitochondrial functions, oxidative stress responses (including tRNA thiouridine modification reprogramming), and an enhanced DNA damage repair mechanism 3, 811, 1320

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