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。
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Data availability statement
The basis of data is obtained from The Human Protein Atlas database (https://www.proteinatlas.org).
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Acknowledgments
This work was supported by the National Natural Science Foundation of China (No. 81970431) and the Hunan Provincial Natural Science Foundation of China (No. 2023JJ50136).
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Conceptualization: Liwen WANG and Li QIN. Resources: Lanfang LI. Data curation: Liwen WANG and Li QIN. Software: Li QIN. Formal analysis: Liwen WANG and Li QIN. Supervision: Lanfang LI and Huimei LIU. Validation: Liwen WANG. Writing — original draft: Liwen WANG and Li QIN. Project administration: Lanfang LI. Writing — review & editing: Liwen WANG. All authors have read and approved the final manuscript, and therefore, have full access to all the data in the study and take responsibility for the integrity and security of the data.
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Liwen WANG, Li QIN, Huimei LIU, and Lanfang LI declare that they have no conflict of interest.
This article does not contain any studies with human or animal subjects performed by any of the authors.
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Wang, L., Qin, L., Liu, H. et al. HPCAL1 is a novel driver of autophagy-dependent ferroptosis. J. Zhejiang Univ. Sci. B 24, 1053–1056 (2023). https://doi.org/10.1631/jzus.B2300241
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DOI: https://doi.org/10.1631/jzus.B2300241