Evidence map›Paper›PMID 41592892›Full record

ArticleJournal for immunotherapy of cancer2026

Targeting AKR1B1 reprograms tumor-associated macrophages to enhance antitumor immunity.

Yuqing Liu, Chao Zhou, Yabin Tang, Huimin Lei, Ayinazhaer Aihemaiti, Hongyu Liu, Peichen Zou, Junting Xie, Xu Guo, Ruixue Xia and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal for immunotherapy of cancer, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. Article
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

13 authors.

Yuqing Liu *Department of Pharmacology and Chemical Biology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID http://orcid.org/0009-0006-1848-9002
Chao Zhou *Department of Respiratory and Critical Care Medicine, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yabin TangDepartment of Pharmacology and Chemical Biology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Huimin LeiDepartment of Pharmacology and Chemical Biology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Ayinazhaer AihemaitiDepartment of Pharmacology and Chemical Biology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Hongyu LiuDepartment of Respiratory and Critical Care Medicine, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Peichen ZouDepartment of Pharmacology and Chemical Biology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Junting XieDepartment of Pharmacology and Chemical Biology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Xu GuoDepartment of Pharmacology and Chemical Biology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Ruixue XiaDepartment of Pharmacology and Chemical Biology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Bao-Hui HanDepartment of Respiratory and Critical Care Medicine, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID http://orcid.org/0000-0003-3534-093X
Hongzhuan ChenShuguang Lab of Future Health, Shanghai Frontiers Science Center of TCM Chemical Biology, Shuguang Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, China julianzhu@sjtu.edu.cn hongzhuan_chen@hotmail.com.
Liang ZhuDepartment of Pharmacology and Chemical Biology, Shanghai Jiao Tong University School of Medicine, Shanghai, China julianzhu@sjtu.edu.cn hongzhuan_chen@hotmail.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTumor-associated macrophages (TAMs) are key drivers of the immunosuppressive tumor microenvironment (TME), thereby limiting the efficacy of immune checkpoint inhibitors (ICIs). However, the underlying mechanisms remain unclear.

methodsBoth genetic (Akr1b3 knockout) and pharmacologic (epalrestat) approaches were employed to examine the impact of Aldo-keto reductase family 1 member B1 (AKR1B1) inhibition on TAMs and T-cell function in vitro and in vivo. Mechanistic insights were obtained through RNA sequencing, flow cytometry, immunofluorescence staining, and co-culture assays. To assess therapeutic relevance, 4T1 breast cancer and LLC lung carcinoma mouse models were used to evaluate the effects of epalrestat on tumor growth, immune infiltration, and T-cell responses. Clinical relevance was validated in patient cohorts with triple-negative breast cancer (TNBC) and lung adenocarcinoma (LUAD).

resultsAKR1B1 is highly expressed in TAMs and correlates with CD8

conclusionsAKR1B1 as a critical regulator of TAM-mediated immunosuppression and highlight its therapeutic potential to enhance the efficacy of ICIs.

Indexed as

Aldehyde ReductaseAldo-Keto ReductasesTumor-Associated MacrophagesAnimalsCell Line, TumorFemaleHumansMiceTumor MicroenvironmentAldehyde ReductaseAldo-Keto ReductasesImmunosuppressionImmunotherapySolid tumorTumor infiltrating lymphocyte - TILTumor microenvironment - TME

Identifiers

PMID41592892
PMCPMC12853464

What OpenQuestion holds

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Registered trials

None linked

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.