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用于癌症治疗的生物活性乳酸脱氢酶纳米平台:调节程序性细胞死亡的研究进展

Bioactive LDH nanoplatforms for cancer therapy: Advances in modulating programmed cell death.

作者信息

Wang Li, Ran Nana, Hu TingTing, Cui Xiaoliang, Kang Yong, Ge Min

机构信息

Academy of Medical Engineering and Translational Medicine, Medical College, Tianjin University, Tianjin, 300072, China.

Department of Electrical Engineering, City University of Hong Kong, Tat Chee Avenue, 999077, Hong Kong Special Administrative Region of China.

出版信息

Mater Today Bio. 2025 Jul 26;34:102139. doi: 10.1016/j.mtbio.2025.102139. eCollection 2025 Oct.


DOI:10.1016/j.mtbio.2025.102139
PMID:40761508
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12320707/
Abstract

In recent years, the rapid advancement of nanotechnology and tumor biology has significantly expanded the application of nanomaterials in cancer therapy, particularly through the induction of programmed cell death (PCD) in cancer cells. Layered double hydroxides (LDH), a class of two-dimensional inorganic nanomaterials, have attracted considerable attention due to its tunable structures, excellent biocompatibility, and superior drug delivery capabilities. Emerging research has highlighted the great potential of LDH in modulating various forms of PCD. In this review, we provide a comprehensive overview of recent progress in the use of LDH to regulate different PCD pathways in cancer cells, including apoptosis, autophagy, ferroptosis, cuproptosis and pyroptosis. It emphasizes the underlying mechanisms of action, material design strategies, and the application of LDH in precise cancer therapy. Finally, this review is concluded with perspectives on the key challenges and bottlenecks of bioactive LDH in cancer therapy, providing potential solutions and outlining future perspectives.

摘要

近年来,纳米技术和肿瘤生物学的迅速发展显著扩大了纳米材料在癌症治疗中的应用,特别是通过诱导癌细胞的程序性细胞死亡(PCD)。层状双氢氧化物(LDH)是一类二维无机纳米材料,因其可调控的结构、优异的生物相容性和卓越的药物递送能力而备受关注。新兴研究突出了LDH在调节各种形式PCD方面的巨大潜力。在本综述中,我们全面概述了使用LDH调节癌细胞中不同PCD途径的最新进展,包括凋亡、自噬、铁死亡、铜死亡和焦亡。它强调了潜在的作用机制、材料设计策略以及LDH在精确癌症治疗中的应用。最后,本综述以对生物活性LDH在癌症治疗中的关键挑战和瓶颈的观点作结,提供了潜在的解决方案并概述了未来的前景。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c2ef/12320707/c4416068eb51/gr9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c2ef/12320707/3867c92ceb1e/ga1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c2ef/12320707/4b4cb9f64f43/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c2ef/12320707/0cf6f3d28506/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c2ef/12320707/c3d96be820ff/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c2ef/12320707/e33247a49812/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c2ef/12320707/2f15eb5968c5/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c2ef/12320707/52419aa8fdea/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c2ef/12320707/a9f142edf8ef/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c2ef/12320707/e3211833b3f9/gr8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c2ef/12320707/c4416068eb51/gr9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c2ef/12320707/3867c92ceb1e/ga1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c2ef/12320707/4b4cb9f64f43/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c2ef/12320707/0cf6f3d28506/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c2ef/12320707/c3d96be820ff/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c2ef/12320707/e33247a49812/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c2ef/12320707/2f15eb5968c5/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c2ef/12320707/52419aa8fdea/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c2ef/12320707/a9f142edf8ef/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c2ef/12320707/e3211833b3f9/gr8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c2ef/12320707/c4416068eb51/gr9.jpg

相似文献

[1]
Bioactive LDH nanoplatforms for cancer therapy: Advances in modulating programmed cell death.

Mater Today Bio. 2025-7-26

[2]
Cuproptosis: a novel therapeutic mechanism in lung cancer.

Cancer Cell Int. 2025-6-24

[3]
Potential value and cardiovascular risks of programmed cell death in cancer treatment.

Front Pharmacol. 2025-7-3

[4]
Molecular subtypes of lung adenocarcinoma patients for prognosis and therapeutic response prediction with machine learning on 13 programmed cell death patterns.

J Cancer Res Clin Oncol. 2023-10

[5]
From mechanism to application: programmed cell death pathways in nanomedicine-driven cancer therapies.

Bioact Mater. 2025-7-1

[6]
Revolutionizing breast cancer treatment: Harnessing the related mechanisms and drugs for regulated cell death (Review).

Int J Oncol. 2024-5

[7]
Nanotechnology-targeted modulation of mitophagy in cancer therapy: Progress and challenges.

Acta Biomater. 2025-7-28

[8]
Management of urinary stones by experts in stone disease (ESD 2025).

Arch Ital Urol Androl. 2025-6-30

[9]
Targeting Ferroptosis With Natural Products to Treat Diabetes and Its Complications: Opportunities and Challenges.

Phytother Res. 2025-7-9

[10]
Greenly Synthesized Manganese Oxide Nanoparticles (MnO NPs) In Tumor Therapy: A Narrative Review.

Arch Razi Inst. 2024-12-31

本文引用的文献

[1]
Cuproptosis: mechanisms and nanotherapeutic strategies in cancer and beyond.

Chem Soc Rev. 2025-6-30

[2]
Layered double hydroxides for regenerative nanomedicine and tissue engineering: recent advances and future perspectives.

J Nanobiotechnology. 2025-5-22

[3]
Engineering pyroptotic vesicles as personalized cancer vaccines.

Nat Nanotechnol. 2025-5-16

[4]
Updated insights into the molecular networks for NLRP3 inflammasome activation.

Cell Mol Immunol. 2025-4-30

[5]
Radiotherapy promotes cuproptosis and synergizes with cuproptosis inducers to overcome tumor radioresistance.

Cancer Cell. 2025-6-9

[6]
p53-regulated non-apoptotic cell death pathways and their relevance in cancer and other diseases.

Nat Rev Mol Cell Biol. 2025-4-9

[7]
Gallium-Magnesium Layered Double Hydroxide for Elevated Tumor Immunotherapy Through Multi-Network Synergistic Regulation.

Adv Mater. 2025-5

[8]
Autophagy in tumor immune escape and immunotherapy.

Mol Cancer. 2025-3-19

[9]
Layered Double Hydroxide LDH-Loaded miR-141-3p Targets RAB10 Suppressing Cellular Autophagy to Reverse Paclitaxel Resistance in Breast Cancer.

ACS Omega. 2025-2-10

[10]
Hydrotalcites-Induced Pyroptosis Combined with Toll-Like Receptor Activation Elicited Dual Stimulation of Innate and Adaptive Immunity.

ACS Nano. 2025-3-4

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