Evidence map›Paper›PMID 39119940›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2024

Surface Molecularly Engineered Mitochondria Conduct Immunophenotype Repolarization of Tumor-Associated Macrophages to Potentiate Cancer Immunotherapy.

Cai-Ju Zhang, Jia-Mi Li, Dan Xu, Dan-Dan Wang, Ming-Hui Qi, Feng Chen, Bo Wu, Kai Deng, Shi-Wen Huang

Abstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 2 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

33 citing papers in PubMed, 2 syntheses or guidelines pooled it.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

Cai-Ju ZhangDepartment of Radiology, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan, 430071, China.
Jia-Mi LiKey Laboratory of Biomedical Polymers of Ministry of Education, Department of Chemistry, Wuhan University, Wuhan, 430072, China.
Dan XuDepartment of Nuclear Medicine, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan, 430071, China.
Dan-Dan WangKey Laboratory of Biomedical Polymers of Ministry of Education, Department of Chemistry, Wuhan University, Wuhan, 430072, China.
Ming-Hui QiKey Laboratory of Biomedical Polymers of Ministry of Education, Department of Chemistry, Wuhan University, Wuhan, 430072, China.
Feng ChenDepartment of Radiology, Hainan Hospital Affiliated to Hainan Medical University, Hainan, 570311, China.
Bo WuDepartment of Radiology, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan, 430071, China.
Kai DengDepartment of Radiology, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan, 430071, China.ORCID 0009-0001-4597-8593
Shi-Wen HuangKey Laboratory of Biomedical Polymers of Ministry of Education, Department of Chemistry, Wuhan University, Wuhan, 430072, China.

Funding

National Natural Science Foundation of China 52173137National Natural Science Foundation of China 52373156National Natural Science Foundation of China 82202132Youth Interdisciplinary Special Fund of Zhongnan Hospital of Wuhan University ZNQNJC2022002
6 · The paper itself

Abstract

Reprogramming tumor-associated macrophages (TAMs) to an inflammatory phenotype effectively increases the potential of immune checkpoint blockade (ICB) therapy. Artificial mitochondrial transplantation, an emerging and safe strategy, has made brilliant achievements in regulating the function of recipient cells in preclinic and clinic, but its performance in reprogramming the immunophenotype of TAMs has not been reported. Here, the metabolism of M2 TAMs is proposed resetting from oxidative phosphorylation (OXPHOS) to glycolysis for polarizing M1 TAMs through targeted transplantation of mannosylated mitochondria (mPEI/M1mt). Mitochondria isolated from M1 macrophages are coated with mannosylated polyethyleneimine (mPEI) through electrostatic interaction to form mPEI/M1mt, which can be targeted uptake by M2 macrophages expressed a high level of mannose receptors. Mechanistically, mPEI/M1mt accelerates phosphorylation of NF-κB p65, MAPK p38 and JNK by glycolysis-mediated elevation of intracellular ROS, thus prompting M1 macrophage polarization. In vivo, the transplantation of mPEI/M1mt excellently potentiates therapeutic effects of anti-PD-L1 by resetting an antitumor proinflammatory tumor microenvironment and stimulating CD8 and CD4 T cells dependent immune response. Altogether, this work provides a novel platform for improving cancer immunotherapy, meanwhile, broadens the scope of mitochondrial transplantation technology in clinics in the future.

Indexed as

ImmunotherapyMitochondriaTumor-Associated MacrophagesAnimalsDisease Models, AnimalHumansImmunophenotypingMiceMice, Inbred C57BLNeoplasmsTumor Microenvironmentimmunotherapymetabolic regulationmitochondrial transplantationsurface molecular engineeringtumor‐associated macrophage

Identifiers

PMID39119940
PMCPMC11481252

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.