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On-line Access: 2024-08-27

Received: 2023-10-17

Revision Accepted: 2024-05-08

Crosschecked: 2023-11-15

Cited: 0

Clicked: 1015

Citations:  Bibtex RefMan EndNote GB/T7714

 ORCID:

Liwen WANG

https://orcid.org/0009-0000-3945-0760

Lanfang LI

https://orcid.org/0000-0001-7510-8751

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Journal of Zhejiang University SCIENCE B 2023 Vol.24 No.11 P.1053-1056

http://doi.org/10.1631/jzus.B2300241


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


Liwen WANG, Li Qin, Huimei LIU, Lanfang LI. HPCAL1 is a novel driver of autophagy-dependent ferroptosis[J]. Journal of Zhejiang University Science B, 2023, 24(11): 1053-1056.

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author="Liwen WANG, Li Qin, Huimei LIU, Lanfang LI",
journal="Journal of Zhejiang University Science B",
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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:自噬;铁死亡;脂质过氧化;海马钙素样1(HPCAL1);钙粘素2(CDH2)

Darkslateblue:Affiliate; Royal Blue:Author; Turquoise:Article

Reference

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