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Article Abstract

Correction for 'Enhanced photothermal-ferroptosis effects based on RBCm-coated PDA nanoparticles for effective cancer therapy' by Hongli Yu , , 2023, , 415-429, https://doi.org/10.1039/D2TB02329F.

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http://dx.doi.org/10.1039/d5tb90131fDOI Listing

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Correction for 'Enhanced photothermal-ferroptosis effects based on RBCm-coated PDA nanoparticles for effective cancer therapy' by Hongli Yu , , 2023, , 415-429, https://doi.org/10.1039/D2TB02329F.

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Combining photothermal therapy (PTT) with chemotherapy shows promise for cancer treatment, but its efficacy is limited by heat shock protein (HSP)-induced thermoresistance and P-glycoprotein (P-gp)-mediated drug efflux. To overcome these challenges, we developed a tumor microenvironment-responsive microneedle platform for synergistic chemotherapy, PTT, and ferroptosis in breast cancer. The system employs Fe-coordinated dihydromyricetin (DMY) nanocarriers encapsulating doxorubicin (DMFD NPs) integrated into a flexible polyvinylpyrrolidone (PVP) microneedle patch.

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Photothermal therapy (PTT) is impeded by limited light penetration depth and cellular heat resistance induced by overexpressed heat shock proteins. Herein, we propose a ferrocene (Fc)-based supramolecular photothermal agent (PTA) to improve the therapeutic efficacy. Cy-Fc/CD-PEG not only had excellent photothermal effect but also possessed the ability to induce ferroptosis and immunotherapy.

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NIR-responsive CuSe@Fc nanoparticles for photothermal- ferroptosis combination therapy in esophageal cancer.

J Nanobiotechnology

May 2025

School of Materials Science and Engineering, The First Affiliated Hospital, College of Clinical Medicine, Henan University of Science and Technology, Luoyang, 471023, China.

Esophageal cancer (EC) represents a highly recurrent and aggressive malignancy within the digestive system. However, conventional therapeutic strategies exhibit notable limitations in their clinical applications. Photothermal therapy (PTT), combined with ferroptosis, has attracted considerable attentions, emerging as a promising novel strategy for EC treatment.

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Cellular defense mechanisms against ferroptosis are primarily mediated by antiferroptotic regulators, particularly glutathione peroxidase 4 (GPX4) and ferroptosis suppressor protein 1 (FSP1). Notably, singlet oxygen (O) generated through photoactivation of organic small-molecule photosensitizers (PSs) has been demonstrated to deplete both glutathione (GSH) and nicotinamide adenine dinucleotide phosphate (NADPH). This dual depletion mechanism effectively disrupts the GSH/GPX4 redox axis and the NADPH/FSP1/ubiquinone (CoQ) antioxidant system, thereby potentiating ferroptosis.

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