Evidence map›Paper›PMID 40696413›Full record

ReviewExperimental hematology & oncology2025

Decoding the metabolic dialogue in the tumor microenvironment: from immune suppression to precision cancer therapies.

Ruoli Wang, Jincheng Zhuang, Qi Zhang, Wantao Wu, Xinrui Yu, Hao Zhang, Zongyi Xie

Abstract readReview
In one paragraph

Review in Experimental hematology & oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Oxycodone combined with pulsed radiofrequency for refractory cancer pain from spinal metastases: a randomized controlled study.Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 2026
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  3. New insights into the ACLY-mediated metabolic and epigenetic interplay in macrophages.Journal of enzyme inhibition and medicinal chemistry · 2026
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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

7 authors.

Ruoli Wang *Department of Neurosurgery, The Second Affiliated Hospital, Chongqing Medical University, Chongqing, China.
Jincheng Zhuang *Department of Neurosurgery, The Second Affiliated Hospital, Chongqing Medical University, Chongqing, China.
Qi Zhang *Department of Neurosurgery, The Second Affiliated Hospital, Chongqing Medical University, Chongqing, China.
Wantao WuDepartment of Thyroid and Breast Surgery, The Second Affiliated Hospital, Chongqing Medical University, Chongqing, China.
Xinrui YuDepartment of Neurosurgery, The Second Affiliated Hospital, Chongqing Medical University, Chongqing, China.
Hao ZhangDepartment of Neurosurgery, The Second Affiliated Hospital, Chongqing Medical University, Chongqing, China. zhsw@hospital.cqmu.edu.cn.
Zongyi XieDepartment of Neurosurgery, The Second Affiliated Hospital, Chongqing Medical University, Chongqing, China. zyxie2008@cqmu.edu.cn.

Funding

Chongqing Medical Leading Talents Program YXLJ202429Chongqing Postdoctoral Science Foundation CSTB2023NSCQBHX0002Kuanren Talents Program of the Second Affiliated Hospital of Chongqing Medical University 20241708National Natural Science Foundation of China 82303610, 82471321Natural Science Foundation Project of Chongqing, Chongqing Science and Technology Commission CSTB2023NSCQ-MSX0107
6 · The paper itself

Abstract

The tumor microenvironment (TME) represents a metabolic battleground where immune cells and cancer cells vie for essential nutrients, ultimately influencing antitumor immunity and treatment outcomes. Recent advancements have shed light on how the metabolic reprogramming of immune cells, including macrophages, T cells, and DCs, determines their functional polarization, survival, and interactions within the TME. Factors such as hypoxia, acidosis, and nutrient deprivation drive immune cells toward immunosuppressive phenotypes, while metabolic interactions between tumors and stromal cells further entrench therapeutic resistance. This review synthesizes new insights into the metabolic checkpoints that regulate immune cell behavior, focusing on processes like glycolysis, oxidative phosphorylation (OXPHOS), lipid oxidation, and amino acid dependencies. We emphasize how metabolic enzymes (e.g., IDO1, ACLY, CPT1A) and metabolites (e.g., lactate, kynurenine) facilitate immune evasion, and we propose strategies to reverse these pathways. Innovations such as single-cell metabolomics, spatial profiling, and AI-driven drug discovery are transforming our understanding of metabolic heterogeneity and its clinical implications. Furthermore, we discuss cutting-edge therapeutic approaches-from dual-targeting metabolic inhibitors to biomaterial-based delivery systems-that aim to reprogram immune cell metabolism and enhance the effectiveness of immunotherapy. Despite the promise in preclinical studies, challenges persist in translating these findings to clinical applications, including biomarker validation, metabolic plasticity, and interpatient variability. By connecting mechanistic discoveries with translational applications, this review highlights the potential of immunometabolic targeting to overcome resistance and redefine precision oncology.

Indexed as

Immune cells metabolismImmunotherapy resistanceMetabolic reprogrammingTherapeutic targetingTumor microenvironment

Identifiers

PMID40696413
PMCPMC12282028

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

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 Socratic graph.