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While nutritional VC intake demonstrates chemopreventive effects by scavenging carcinogen-induced reactive oxygen species (ROS) and maintaining genomic stability, high-dose intravenous VC acts as a prooxidant to selectively kill tumor cells via ROS-mediated deoxyribonucleic acid (DNA) damage, adenosine triphosphate (ATP) depletion, and HIF-1 degradation

Reduced FAK-STAT3 signaling contributes to ER stress-induced mitochondrial dysfunction and death in endothelial cells

The authors would like to acknowledge the research team in the Department of Tissue Engineering and Regenerative Medicine (DTERM), Faculty of Medicine, Universiti Kebangsaan Malaysia, for the technical support throughout this review

doi:10.1002/advs.202405620 19

Together, let's embrace this powerful antioxidant as part of our commitment to a healthier future.