HPCAL1 is a novel driver of autophagy-dependent ferroptosis
Liwen WANG, Li Qin, Huimei LIU, Lanfang LI
Institute of Pharmaceutical Pharmacology, School of Pharmacy, University of South China, Hengyang 421001, China; Hengyang Medical School, University of South China, Hengyang 421001, China
llanfang6@126.com
Abstract: Autophagy is a highly conserved physiological process in cells that degrades excess or damaged organelles, large protein aggregates, and pathogens via the lysosomal system (Li et al., 2021). Autophagy generally increases the self-protection mechanism of cells, which plays an important role in the maintenance of cell homeostasis as well as the synthesis, degradation, and recycling of cell products. However, in certain circumstances, activation of autophagy or excessive autophagy can lead to cell death, a phenomenon called autophagy-dependent cell death (Liu et al., 2020). Recent research has found that, under certain conditions, autophagy activation or excessive autophagy can regulate ferroptosis through corresponding mechanisms (Xie et al., 2023).