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基于纳米颗粒的铁死亡、细胞焦亡和自噬在癌症免疫治疗中的应用。

The application of nanoparticles-based ferroptosis, pyroptosis and autophagy in cancer immunotherapy.

机构信息

Department of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.

Department of Geriatric Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.

出版信息

J Nanobiotechnology. 2024 Mar 7;22(1):97. doi: 10.1186/s12951-024-02297-8.


DOI:10.1186/s12951-024-02297-8
PMID:38454419
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10921615/
Abstract

Immune checkpoint blockers (ICBs) have been applied for cancer therapy and achieved great success in the field of cancer immunotherapy. Nevertheless, the broad application of ICBs is limited by the low response rate. To address this issue, increasing studies have found that the induction of immunogenic cell death (ICD) in tumor cells is becoming an emerging therapeutic strategy in cancer treatment, not only straightly killing tumor cells but also enhancing dying cells immunogenicity and activating antitumor immunity. ICD is a generic term representing different cell death modes containing ferroptosis, pyroptosis, autophagy and apoptosis. Traditional chemotherapeutic agents usually inhibit tumor growth based on the apoptotic ICD, but most tumor cells are resistant to the apoptosis. Thus, the induction of non-apoptotic ICD is considered to be a more efficient approach for cancer therapy. In addition, due to the ineffective localization of ICD inducers, various types of nanomaterials have been being developed to achieve targeted delivery of therapeutic agents and improved immunotherapeutic efficiency. In this review, we briefly outline molecular mechanisms of ferroptosis, pyroptosis and autophagy, as well as their reciprocal interactions with antitumor immunity, and then summarize the current progress of ICD-induced nanoparticles based on different strategies and illustrate their applications in the cancer therapy.

摘要

免疫检查点抑制剂 (ICBs) 已被应用于癌症治疗,并在癌症免疫治疗领域取得了巨大成功。然而,ICBs 的广泛应用受到低反应率的限制。为了解决这个问题,越来越多的研究发现,诱导肿瘤细胞发生免疫原性细胞死亡 (ICD) 正在成为癌症治疗的一种新兴治疗策略,不仅可以直接杀死肿瘤细胞,还可以增强死亡细胞的免疫原性并激活抗肿瘤免疫。ICD 是代表不同细胞死亡模式的通用术语,包括铁死亡、细胞焦亡、自噬和细胞凋亡。传统的化疗药物通常基于凋亡 ICD 抑制肿瘤生长,但大多数肿瘤细胞对凋亡具有抗性。因此,诱导非凋亡 ICD 被认为是一种更有效的癌症治疗方法。此外,由于 ICD 诱导剂的定位效果不佳,各种类型的纳米材料被开发出来以实现治疗剂的靶向递送和提高免疫治疗效率。在这篇综述中,我们简要概述了铁死亡、细胞焦亡和自噬的分子机制,以及它们与抗肿瘤免疫的相互作用,然后总结了基于不同策略的 ICD 诱导纳米颗粒的最新进展,并说明了它们在癌症治疗中的应用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b32f/10921615/c9d7dac342f3/12951_2024_2297_Fig13_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b32f/10921615/a83cfc70c9f6/12951_2024_2297_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b32f/10921615/0785a9a336cf/12951_2024_2297_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b32f/10921615/b46c9a4b1f88/12951_2024_2297_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b32f/10921615/b8d388c8467c/12951_2024_2297_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b32f/10921615/4589ddc2765e/12951_2024_2297_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b32f/10921615/99aafb28039b/12951_2024_2297_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b32f/10921615/d0feaec132b6/12951_2024_2297_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b32f/10921615/5b1b818c8163/12951_2024_2297_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b32f/10921615/7b5c8edd8b27/12951_2024_2297_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b32f/10921615/18b73fb60710/12951_2024_2297_Fig10_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b32f/10921615/bbc0c7d1aa8d/12951_2024_2297_Fig11_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b32f/10921615/3324b4523b9b/12951_2024_2297_Fig12_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b32f/10921615/c9d7dac342f3/12951_2024_2297_Fig13_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b32f/10921615/a83cfc70c9f6/12951_2024_2297_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b32f/10921615/0785a9a336cf/12951_2024_2297_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b32f/10921615/b46c9a4b1f88/12951_2024_2297_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b32f/10921615/b8d388c8467c/12951_2024_2297_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b32f/10921615/4589ddc2765e/12951_2024_2297_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b32f/10921615/99aafb28039b/12951_2024_2297_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b32f/10921615/d0feaec132b6/12951_2024_2297_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b32f/10921615/5b1b818c8163/12951_2024_2297_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b32f/10921615/7b5c8edd8b27/12951_2024_2297_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b32f/10921615/18b73fb60710/12951_2024_2297_Fig10_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b32f/10921615/bbc0c7d1aa8d/12951_2024_2297_Fig11_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b32f/10921615/3324b4523b9b/12951_2024_2297_Fig12_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b32f/10921615/c9d7dac342f3/12951_2024_2297_Fig13_HTML.jpg

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