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231226s2022 xx |||||o 00| ||eng c |
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|a 10.1002/adma.202206121
|2 doi
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|a pubmed25n1150.xml
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|a (NLM)36017886
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|a DE-627
|b ger
|c DE-627
|e rakwb
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|a eng
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|a Liu, Yu
|e verfasserin
|4 aut
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|a Tumor Selective Metabolic Reprogramming as a Prospective PD-L1 Depression Strategy to Reactivate Immunotherapy
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|c 2022
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|a Text
|b txt
|2 rdacontent
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|a ƒaComputermedien
|b c
|2 rdamedia
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|a ƒa Online-Ressource
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|2 rdacarrier
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|a Date Completed 17.10.2022
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|a Date Revised 20.03.2023
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|a published: Print-Electronic
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|a Citation Status MEDLINE
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|a © 2022 Wiley-VCH GmbH.
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|a Currently, the role of the lysosome, endoplasmic reticulum, or dictyosome in the transcription and translation of programmed cell death ligand 1 (PD-L1) is well revealed, but the role and function of mitochondria in the PD-L1 expression in tumors is still not fully researched, making it hard to offer a novel PD-L1 regulation strategy. In this research, it is newly revealed that mitochondria oxidative phosphorylation (OXPHOS) depression can be used as an effective PD-L1 down-regulation method. To offer an ideal and high-effective tumor mitochondria-targeted OXPHOS depression nanosystem, IR-LND is prepared by conjugating mitochondria-targeted heptamethine cyanine dye IR-68 with mitochondrial complexes I and II depression agent lonidamine (LND), which then further self-assembled with albumin (Alb) to form IR-LNDAlb nanoparticles. By doing this, PD-L1 expression in tumors is selectively and effectively depressed by IR-LND@Alb nanoparticles. As expected, the anti-tumor efficacy of such a PD-L1 depression strategy is superior to conventional anti-PD-L1 monoclonal antibodies. Interestingly, IR-LND can also be served as a novel ideal promising photodynamic therapy (PDT) drug with self-oxygen and self-PD-L1 regulation capacity. All in all, this tumor-selective metabolic reprogramming platform to reactivate immunotherapy and sensitize for PDT effect, would open a new window for mitochondrial immunotherapy for cancer patients
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|a Journal Article
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|a immunotherapy
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|a mitochondria
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|a photodynamic therapy
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|a programmed death ligand-1
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|a tumor targeting
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|a Albumins
|2 NLM
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|a Antibodies, Monoclonal
|2 NLM
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|a B7-H1 Antigen
|2 NLM
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|a Carbocyanines
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|a Immunologic Factors
|2 NLM
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|a Ligands
|2 NLM
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|a Programmed Cell Death 1 Receptor
|2 NLM
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|a heptamethine cyanine dye
|2 NLM
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|a Oxygen
|2 NLM
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|a S88TT14065
|2 NLM
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|a Zhou, Zaigang
|e verfasserin
|4 aut
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1 |
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|a Hou, Jiting
|e verfasserin
|4 aut
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1 |
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|a Xiong, Wei
|e verfasserin
|4 aut
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|a Kim, Heejeong
|e verfasserin
|4 aut
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|a Chen, Jiashe
|e verfasserin
|4 aut
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1 |
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|a Zheng, Chunjuan
|e verfasserin
|4 aut
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|a Jiang, Xin
|e verfasserin
|4 aut
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|a Yoon, Juyoung
|e verfasserin
|4 aut
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|a Shen, Jianliang
|e verfasserin
|4 aut
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|i Enthalten in
|t Advanced materials (Deerfield Beach, Fla.)
|d 1998
|g 34(2022), 41 vom: 01. Okt., Seite e2206121
|w (DE-627)NLM098206397
|x 1521-4095
|7 nnas
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|g volume:34
|g year:2022
|g number:41
|g day:01
|g month:10
|g pages:e2206121
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|u http://dx.doi.org/10.1002/adma.202206121
|3 Volltext
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|d 34
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|e 41
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