Evidence map›Paper›PMID 41736012›Full record

ReviewJournal of translational medicine2026

Mitophagy-driven multidimensional regulation of tumor immune evasion and context-dependent therapeutic strategies.

Xinyi Tan, Jintong Na, Xiaorui Tian, Rui Zhu, Yongjie Su, Yongbin Chen, Liping Zhong

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Journal of translational medicine, 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

7 authors.

Xinyi Tan *State Key Laboratory of Targeting Oncology, National Center for International Research of Bio-Targeting Theranostics, Guangxi Key Laboratory of Bio-Targeting Theranostics, Collaborative Innovation Center for Targeting Tumor Diagnosis and Therapy, Guangxi Talent Highland of Major New Drugs Innovation and Development, Targeting Theranostics Research Center of Guangxi Higher Education, Guangxi Medical University, Nanning, Guangxi, 530021, China.
Jintong Na *State Key Laboratory of Targeting Oncology, National Center for International Research of Bio-Targeting Theranostics, Guangxi Key Laboratory of Bio-Targeting Theranostics, Collaborative Innovation Center for Targeting Tumor Diagnosis and Therapy, Guangxi Talent Highland of Major New Drugs Innovation and Development, Targeting Theranostics Research Center of Guangxi Higher Education, Guangxi Medical University, Nanning, Guangxi, 530021, China.
Xiaorui TianState Key Laboratory of Targeting Oncology, National Center for International Research of Bio-Targeting Theranostics, Guangxi Key Laboratory of Bio-Targeting Theranostics, Collaborative Innovation Center for Targeting Tumor Diagnosis and Therapy, Guangxi Talent Highland of Major New Drugs Innovation and Development, Targeting Theranostics Research Center of Guangxi Higher Education, Guangxi Medical University, Nanning, Guangxi, 530021, China.
Rui ZhuState Key Laboratory of Targeting Oncology, National Center for International Research of Bio-Targeting Theranostics, Guangxi Key Laboratory of Bio-Targeting Theranostics, Collaborative Innovation Center for Targeting Tumor Diagnosis and Therapy, Guangxi Talent Highland of Major New Drugs Innovation and Development, Targeting Theranostics Research Center of Guangxi Higher Education, Guangxi Medical University, Nanning, Guangxi, 530021, China.
Yongjie SuState Key Laboratory of Targeting Oncology, National Center for International Research of Bio-Targeting Theranostics, Guangxi Key Laboratory of Bio-Targeting Theranostics, Collaborative Innovation Center for Targeting Tumor Diagnosis and Therapy, Guangxi Talent Highland of Major New Drugs Innovation and Development, Targeting Theranostics Research Center of Guangxi Higher Education, Guangxi Medical University, Nanning, Guangxi, 530021, China.
Yongbin ChenState Key Laboratory of Targeting Oncology, National Center for International Research of Bio-Targeting Theranostics, Guangxi Key Laboratory of Bio-Targeting Theranostics, Collaborative Innovation Center for Targeting Tumor Diagnosis and Therapy, Guangxi Talent Highland of Major New Drugs Innovation and Development, Targeting Theranostics Research Center of Guangxi Higher Education, Guangxi Medical University, Nanning, Guangxi, 530021, China. ybchen@mail.kiz.ac.cn.
Liping ZhongState Key Laboratory of Targeting Oncology, National Center for International Research of Bio-Targeting Theranostics, Guangxi Key Laboratory of Bio-Targeting Theranostics, Collaborative Innovation Center for Targeting Tumor Diagnosis and Therapy, Guangxi Talent Highland of Major New Drugs Innovation and Development, Targeting Theranostics Research Center of Guangxi Higher Education, Guangxi Medical University, Nanning, Guangxi, 530021, China. zhongliping@gxmu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMitophagy is a core component of MQC that maintains metabolic homeostasis and undergoes threshold-dependent dysregulation within the TME. Under hypoxia, nutrient deprivation, and metabolic stress, mitophagy not only supports tumor cell survival but also profoundly modulates antitumor immunity by reshaping immune cell metabolism, mitochondrial signaling, and epigenetic regulation.

methodsThis review integrates findings from molecular biology, metabolomics, and tumor immunology to elucidate the bidirectional immunoregulatory roles of mitophagy. Key signaling axes, including cGAS-STING, JAK-STAT, NF-κB, and HIF-1α/PD-L1, are highlighted, alongside lineage-specific effects of mitophagy in T cells, B cells, NK cells, and TAMs. Therapeutic strategies targeting PINK1/Parkin, BNIP3/FUNDC1, and OPTN-TBK1 pathways are critically discussed.

resultsBoth insufficient and excessive mitophagy disrupt immune homeostasis and promote immunosuppression through distinct mechanisms. Mitophagy deficiency leads to mtROS and mtDNA accumulation, aberrant inflammatory signaling, and functional exhaustion of T cells, B cells, and NK cells. Conversely, excessive mitophagy eliminates mitochondrial danger signals, suppresses cGAS-STING and NF-κB activation, and enhances HIF-1α/STAT3-driven PD-L1 expression. Mitophagy further enforces immune exhaustion via metabolic-epigenetic coupling.

conclusionsMitophagy is a context dependent, immune lineage specific regulatory hub linking metabolic reprogramming, immune signaling attenuation, and epigenetic remodeling. As a dynamic, tunable axis, its rational modulation may overcome tumor immune evasion and therapeutic resistance.

Indexed as

MitophagyNeoplasmsTumor EscapeAnimalsHumansSignal TransductionImmune evasionImmunometabolic reprogrammingImmunotherapy resistanceMetabolic epigeneticsMitophagy

Identifiers

PMID41736012
PMCPMC12964651

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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.