CLC number:
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
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.
@article{title="HPCAL1 is a novel driver of autophagy-dependent ferroptosis",
author="Liwen WANG, Li Qin, Huimei LIU, Lanfang LI",
journal="Journal of Zhejiang University Science B",
volume="24",
number="11",
pages="1053-1056",
year="2023",
publisher="Zhejiang University Press & Springer",
doi="10.1631/jzus.B2300241"
}
%0 Journal Article
%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
%V 24
%N 11
%P 1053-1056
%@ 1673-1581
%D 2023
%I Zhejiang University Press & Springer
%DOI 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
VL - 24
IS - 11
SP - 1053
EP - 1056
%@ 1673-1581
Y1 - 2023
PB - Zhejiang University Press & Springer
ER -
DOI - 10.1631/jzus.B2300241
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 (
[1]BaiYS, MengLJ, HanL, et al., 2019. Lipid storage and lipophagy regulates ferroptosis. Biochem Biophys Res Commun, 508(4):997-1003.
[2]BaoZ, HuaL, YeY, et al., 2021. MEF2C silencing downregulates NF2 and E-cadherin and enhances Erastin-induced ferroptosis in meningioma. Neuro Oncol, 23:2014-2027. http://dx.doi.org/10.1093/neuonc/noab114
[3]ChenX, KangR, KroemerG, et al., 2021. Ferroptosis in infection, inflammation, and immunity. J Exp Med, 218(6):e20210518.
[4]ChenX, SongXX, LiJB, et al., 2023. Identification of HPCAL1 as a specific autophagy receptor involved in ferroptosis. Autophagy, 19(1):54-74.
[5]HouW, XieYC, SongXX, et al., 2016. Autophagy promotes ferroptosis by degradation of ferritin. Autophagy, 12(8):1425-1428.
[6]LiW, HePC, HuangYG, et al., 2021. Selective autophagy of intracellular organelles: recent research advances. Theranostics, 11(1):222-256.
[7]LiuJ, KuangFM, KroemerG, et al., 2020. Autophagy-dependent ferroptosis: machinery and regulation. Cell Chem Biol, 27(4):420-435.
[8]QinX, ZhangJ, WangB, et al., 2021. Ferritinophagy is involved in the zinc oxide nanoparticles-induced ferroptosis of vascular endothelial cells. Autophagy, 17(12):4266-4285.
[9]RuQ, LiYS, XieWQ, et al., 2023. Fighting age-related orthopedic diseases: focusing on ferroptosis. Bone Res, 11(1):12.
[10]TangWY, MoreyLM, CheungYY, et al., 2012. Neonatal exposure to estradiol/bisphenol A alters promoter methylation and expression of Nsbp1 and Hpcal1 genes and transcriptional programs of Dnmt3a/b and Mbd2/4 in the ratprostate gland throughout life. Endocrinology, 153(1):42-55.
[11]WangXY, XieXM, ZhangYY, et al., 2022. Hippocalcin-like 1 is a key regulator of LDHA activation that promotes the growth of non-small cell lung carcinoma. Cell Oncol, 45(1):179-191.
[12]WuZM, GengY, LuXJ, et al., 2019. Chaperone-mediated autophagy is involved in the execution of ferroptosis. Proc Natl Acad Sci USA, 116(8):2996-3005.
[13]XieYC, HouT, LiuJY, et al., 2023. Autophagy-dependent ferroptosis as a potential treatment for glioblastoma. Front Oncol, 13:1091118.
[14]YangMH, ChenP, LiuJ, et al., 2019. Clockophagy is a novel selective autophagy process favoring ferroptosis. Sci Adv, 5(7):eaaw2238.
[15]ZhangDM, LiuXD, XuXB, et al., 2019. HPCAL1 promotes glioblastoma proliferation via activation of Wnt/β-catenin signalling pathway. J Cell Mol Med, 23(5):3108-3117.
[16]ZhangYL, LiuYF, DuanJL, et al., 2016. Hippocalcin-like 1 suppresses hepatocellular carcinoma progression by promoting p21Waf/Cip1 stabilization by activating the ERK1/2-MAPK pathway. Hepatology, 63(3):880-897.
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