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Moreover, in models of ischemiareperfusion injury and in KEAP1-inactivated lung cancer, inhibition or genetic ablation of CoQ biosynthetic enzymes restored sensitivity to ferroptosis or radiotherapy 115,116 , underscoring the reliance of some cancer cells on an abundant CoQ pool for redox defense and survival

This heightened oxidative burden extends beyond immune cells to the airway epithelial cells, which are primary sites of CFTR dysfunction (Regelmann et al., 1991)

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A single temperature excursion

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