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Inhibiting COX-2 attenuated the rise of COX-2 levels and epithelial-mesenchymal transition (EMT) scores in NPC cells driven by MDSCs, suggesting COX-2 as a critical checkpoint for MDSCtumor cell interactions and tumor promotion [47]

This supports that ATP requirements escalate in repair mechanisms due to oxidative damage 17

Expression of vascular endothelial growth factor receptors in the human endometrium: modulation during the menstrual cycle

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ER stress leads to the activation of three ER-resident transmembrane proteins: activating transcription factor-6 (ATF6), inositol requiring protein-1 (IRE1) and protein kinase RNA-like ER kinase (PERK) (Wongprayoon and Govitrapong, 2017)

178 Furthermore, ceramide-mediated mitophagy is upregulated upon PINK1 deficiency, suggesting a compensatory mechanism for maintenance of mitochondrial quality control