JZUS - Journal of Zhejiang University SCIENCE

Journal of Zhejiang University SCIENCE B

Accepted manuscript available online (unedited version)

HPCAL1 is a novel driver of autophagy-dependent ferroptosis

Author(s): Liwen WANG, Li Qin, Huimei LIU, Lanfang LI
Affiliation(s): Institute of Pharmaceutical Pharmacology, School of Pharmacy, University of South China, Hengyang 421001, China; more
Corresponding email(s): llanfang6@126.com
Key Words: Autophagy; Ferroptosis; Lipid peroxidation; HPCAL1; CDH2

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Liwen WANG, Li Qin, Huimei LIU, Lanfang LI. HPCAL1 is a novel driver of autophagy-dependent ferroptosis[J]. Journal of Zhejiang University Science B,in press.Frontiers of Information Technology & Electronic Engineering,in press.https://doi.org/10.1631/jzus.B2300241

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author="Liwen WANG, Li Qin, Huimei LIU, Lanfang LI",
journal="Journal of Zhejiang University Science B",
year="in press",
publisher="Zhejiang University Press & Springer",
doi="https://doi.org/10.1631/jzus.B2300241"
}

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%T HPCAL1 is a novel driver of autophagy-dependent ferroptosis
%A Liwen WANG
%A Li Qin
%A Huimei LIU
%A Lanfang LI
%J Journal of Zhejiang University SCIENCE B
%P 1053-1056
%@ 1673-1581
%D in press
%I Zhejiang University Press & Springer
doi="https://doi.org/10.1631/jzus.B2300241"

TY - JOUR
T1 - HPCAL1 is a novel driver of autophagy-dependent ferroptosis
A1 - Liwen WANG
A1 - Li Qin
A1 - Huimei LIU
A1 - Lanfang LI
J0 - Journal of Zhejiang University Science B
SP - 1053
EP - 1056
%@ 1673-1581
Y1 - in press
PB - Zhejiang University Press & Springer
ER -
doi="https://doi.org/10.1631/jzus.B2300241"

Abstract
Chinese Summary
Academic Network
Reviewer Comment

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).

海马钙素样1是一种新的自噬依赖性铁死亡驱动因子

王丽雯¹，李琴¹，刘惠美²，李兰芳¹
¹南华大学药学院药物药理研究所，中国衡阳市，421001
²南华大学衡阳医学院，中国衡阳市，421001
摘要：自噬是细胞内一种高度保守的生理过程，可通过溶酶体系统降解过量或受损的细胞器、有毒的蛋白聚集体和病原体等。最新研究表明，海马钙素样1（HPCAL1）可作为特异性自噬受体和铁死亡的正调节因子。HPCAL1可选择性降解钙粘素2（CDH2），加速脂质过氧化，促进癌细胞铁死亡。iHPCAL1是抑制HPCAL1的小分子化合物，可抑制Erastin诱导的肿瘤细胞铁死亡。此外，它还可以抑制铁死亡诱导的急性胰腺炎。本文通过对HPCAL1在铁死亡中的具体作用机制进行概述，为HPCAL1作为铁死亡相关疾病的潜在治疗靶点提供新思路和理论依据。

关键词组：自噬；铁死亡；脂质过氧化；海马钙素样1（HPCAL1）；钙粘素2（CDH2）

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Reference

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海马钙素样1是一种新的自噬依赖性铁死亡驱动因子

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