Evidence map›Paper›PMID 41916961›Full record

ArticleCell death discovery2026

Doxorubicin promotes the production of inflammatory cytokines in tumor-associated macrophages through activating lactate dehydrogenase A.

Bin Liu, Wei Yang, Shuo Feng, Xingning Jiang, Jingfan Lu, Fei Wang, Yaowen Hu, Yanhao Liu, Haifeng Ma, Ting Sun

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death discovery, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–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

1 citing paper in PubMed.

  1. Review
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

10 authors.

Bin LiuNeurosurgery and Brain and Nerve Research Laboratory, First Affiliated Hospital of Soochow University, Suzhou, China.
Wei YangState Key Laboratory of Radiation Medicine and Protection, School of Radiation Medicine and Protection and Collaborative Innovation Center of Radiation Medicine of Jiangsu Higher Education Institutions, Soochow University, Suzhou, China. yangwei1976@suda.edu.cn.
Shuo FengNeurosurgery and Brain and Nerve Research Laboratory, First Affiliated Hospital of Soochow University, Suzhou, China.
Xingning JiangState Key Laboratory of Radiation Medicine and Protection, School of Radiation Medicine and Protection and Collaborative Innovation Center of Radiation Medicine of Jiangsu Higher Education Institutions, Soochow University, Suzhou, China.
Jingfan LuState Key Laboratory of Radiation Medicine and Protection, School of Radiation Medicine and Protection and Collaborative Innovation Center of Radiation Medicine of Jiangsu Higher Education Institutions, Soochow University, Suzhou, China.
Fei WangNeurosurgery and Brain and Nerve Research Laboratory, First Affiliated Hospital of Soochow University, Suzhou, China.
Yaowen HuState Key Laboratory of Radiation Medicine and Protection, School of Radiation Medicine and Protection and Collaborative Innovation Center of Radiation Medicine of Jiangsu Higher Education Institutions, Soochow University, Suzhou, China.
Yanhao LiuState Key Laboratory of Radiation Medicine and Protection, School of Radiation Medicine and Protection and Collaborative Innovation Center of Radiation Medicine of Jiangsu Higher Education Institutions, Soochow University, Suzhou, China.
Haifeng MaDepartment of Neurosurgery, Qinghai Provincial People's Hospital, Xining, China. 1344830067@qq.com.
Ting SunNeurosurgery and Brain and Nerve Research Laboratory, First Affiliated Hospital of Soochow University, Suzhou, China. sunting@suda.edu.cn.ORCID http://orcid.org/0000-0001-8287-0541

Funding

National Natural Science Foundation of China (National Science Foundation of China) 32171234
6 · The paper itself

Abstract

Glioblastoma (GBM) presents a significant challenge because of its immunosuppressive microenvironment. The standard treatment protocol, including surgery, radiotherapy, and temozolomide, has been unable to alleviate immunosuppression. Doxorubicin chemotherapy induces immunogenic cell death in cancer cells, reshaping an immune-activated microenvironment. Here, we investigated the mechanism of immune activation induced by doxorubicin in tumor-associated macrophages (TAMs). Radiotherapy and temozolomide plus doxorubicin inhibited tumor growth and reduced the levels of immunosuppressive markers. Mechanically, doxorubicin promotes the production of lactate through activating lactate dehydrogenase A (LDHA) to upregulate the transcription of inflammatory cytokines. Our study confirmed a new mechanism by which doxorubicin remodels the tumor microenvironment by promoting the glycolytic process and lactic acid production, suggesting that combining radiotherapy and temozolomide with doxorubicin chemotherapy may be a potential strategy for GBM treatment.

Identifiers

PMID41916961
PMCPMC13158295

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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.