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Glutathione (GSH) metabolism plays a vital role in the GPX4-dependent antioxidant pathway, whereas CoQ regeneration serves as a cornerstone in non-GPX4 dependent antioxidant pathways ( Figure 2 2.2.1 The canonical GPX4-regulated ferroptosis pathway GPX4, a selenoprotein essential for cellular redox homeostasis, neutralizes PLOOHs on biological membranes by utilizing GSH as its obligate co-substrate ( - , a heterodimeric complex composed of Solute Carrier Family 7 Member 11 (SLC7A11) and Solute Carrier Family 3 Member 2 (SLC3A2), mediates cystine uptake in exchange for intracellular glutamate efflux ( - , encompassing targeted reduction of SLC7A11 levels, inhibition of SLC7A11 degradation and promotion of SLC7A11 expression, indicating that transporter XC - can determine the susceptibility to ferroptosis ( Paradoxically, upon GPX4 ablation, some cancer cell lineages remain resistant to ferroptosis revealing the existence of compensatory GPX4 independent defense mechanisms ( 2.2.2 GPX4-independent surveillance pathways Emerging research has established the Ferroptosis inhibitor protein 1 (FSP1)- Ubiquinone (CoQ) axis as a parallel antioxidant system that functions as a compensatory mechanism specifically in GPX4-deficient cellular contexts ( Recent studies have positioned GTP cyclohydroxylase-1 (GCH1) as another critical regulator of ferroptosis ( A recent study uncovered a mitochondria-localized antioxidant system mediated by Dihydroorotate Dehydrogenase (DHODH) capable of compensating for GPX4 deficiency by neutralizing lipid peroxidation within mitochondria ( In addition, the crosstalk between ferroptosis and other signaling pathways has only been extensively studied in cancer
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Incidence of chronic obstructive pulmonary disease in people with HIV, their parents and siblings in Denmark
