Evidence map›Paper›PMID 34272364›Full record

ArticleNature communications2021

Glucose limitation activates AMPK coupled SENP1-Sirt3 signalling in mitochondria for T cell memory development.

Jianli He, Xun Shangguan, Wei Zhou, Ying Cao, Quan Zheng, Jun Tu, Gaolei Hu, Zi Liang, Cen Jiang, Liufu Deng and 18 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers.

0numbers the graph read from it
0cells of the map it votes in
98citing papers in PubMed
13.0field-weighted citation impact, top 1% of its field
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

98 citing papers in PubMed, 132 citations in OpenAlex.

  1. Review
  2. Mitochondrial dynamics and T cells immunity in cancer.Biochemistry and biophysics reports · 2026
    Review
  3. Article
  4. Targeting PKM2 Enhances the Anti-Tumor Function of CD8International journal of molecular sciences · 2026
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  6. Stress Hyperglycemia Drives CD4Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  7. Article
  8. Review
  9. Adaptive resistance in cancer immunotherapy.Cellular & molecular immunology · 2026
    Review
  10. [SENP1 reduces ferroptosis of thyroid cancer cells by regulating hypoxia-inducible factor-1α].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026
    Article
  11. Article
  12. Review
  13. Review
  14. Post-Translational Regulation of CD8Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Review
  15. Review
  16. Review
  17. Article
  18. SUMOylation protects against sepsis-associated acute kidney injury by stabilizing IκBα.Molecular therapy : the journal of the American Society of Gene Therapy · 2026
    Article
  19. Article
  20. Review

38 more citing papers are in PubMed but not listed here.

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

28 authors at 5 institutions in 1 country.

Jianli He *State Key Laboratory of Oncogenes and Related Genes, Renji Hospital Affiliated; Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Department of Biochemistry and Molecular Cell Biology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Xun Shangguan *Department of Urology, Renji Hospital Affiliated, Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID 0000-0002-6193-0805
Wei ZhouState Key Laboratory of Oncogenes and Related Genes, Renji Hospital Affiliated; Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Department of Biochemistry and Molecular Cell Biology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Ying CaoState Key Laboratory of Oncogenes and Related Genes, Renji Hospital Affiliated; Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Department of Biochemistry and Molecular Cell Biology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Quan ZhengState Key Laboratory of Oncogenes and Related Genes, Renji Hospital Affiliated; Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Department of Biochemistry and Molecular Cell Biology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Jun TuState Key Laboratory of Oncogenes and Related Genes, Renji Hospital Affiliated; Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Department of Biochemistry and Molecular Cell Biology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Gaolei HuState Key Laboratory of Oncogenes and Related Genes, Renji Hospital Affiliated; Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Department of Biochemistry and Molecular Cell Biology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Zi LiangState Key Laboratory of Oncogenes and Related Genes, Renji Hospital Affiliated; Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Department of Biochemistry and Molecular Cell Biology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Cen JiangState Key Laboratory of Oncogenes and Related Genes, Renji Hospital Affiliated; Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Department of Biochemistry and Molecular Cell Biology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Liufu DengDepartment of Urology, Xinhua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID 0000-0002-1164-6777
Shengdian WangInstitute of Biophysics, Chinese Academy of Sciences, Beijing, China.
Wen YangState Key Laboratory of Oncogenes and Related Genes, Renji Hospital Affiliated; Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Department of Biochemistry and Molecular Cell Biology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yong ZuoState Key Laboratory of Oncogenes and Related Genes, Renji Hospital Affiliated; Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Department of Biochemistry and Molecular Cell Biology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Jiao MaState Key Laboratory of Oncogenes and Related Genes, Renji Hospital Affiliated; Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Department of Biochemistry and Molecular Cell Biology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Rong CaiState Key Laboratory of Oncogenes and Related Genes, Renji Hospital Affiliated; Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Department of Biochemistry and Molecular Cell Biology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yalan ChenState Key Laboratory of Oncogenes and Related Genes, Renji Hospital Affiliated; Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Department of Biochemistry and Molecular Cell Biology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Qiuju FanState Key Laboratory of Oncogenes and Related Genes, Renji Hospital Affiliated; Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Department of Biochemistry and Molecular Cell Biology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Baijun DongDepartment of Urology, Renji Hospital Affiliated, Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID 0000-0002-5721-9586
Wei XueDepartment of Urology, Renji Hospital Affiliated, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Hongsheng TanClinical Research Center, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yitao QiCollege of Life Sciences, Shaanxi Normal University, Xi'an, Shaanxi, China.
Jianmin GuDepartment of Thoracic Surgery, Zhongshan Hospital, Fudan University, Shanghai, China.
Bing SuShanghai Institute of Immunology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Y Eugene ChinInstitutes of Biology and Medical Sciences, Soochow University Medical College, Suzhou, Jiangsu, China.
Guoqiang ChenState Key Laboratory of Oncogenes and Related Genes, Renji Hospital Affiliated; Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Department of Biochemistry and Molecular Cell Biology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID 0000-0003-4936-2363
Qi WangDepartment of Urology, Renji Hospital Affiliated, Shanghai Jiao Tong University School of Medicine, Shanghai, China. wqi@sjtu.edu.cn.
Tianshi WangState Key Laboratory of Oncogenes and Related Genes, Renji Hospital Affiliated; Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Department of Biochemistry and Molecular Cell Biology, Shanghai Jiao Tong University School of Medicine, Shanghai, China. tianshi777@shsmu.edu.cn.
Jinke ChengState Key Laboratory of Oncogenes and Related Genes, Renji Hospital Affiliated; Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Department of Biochemistry and Molecular Cell Biology, Shanghai Jiao Tong University School of Medicine, Shanghai, China. jkcheng@shsmu.edu.cn.ORCID 0000-0002-4344-5363
Shanghai Jiao Tong University · CNChinese Academy of Sciences · CNShaanxi Normal University · CNSoochow University · CNSun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metabolic programming and mitochondrial dynamics along with T cell differentiation affect T cell fate and memory development; however, how to control metabolic reprogramming and mitochondrial dynamics in T cell memory development is unclear. Here, we provide evidence that the SUMO protease SENP1 promotes T cell memory development via Sirt3 deSUMOylation. SENP1-Sirt3 signalling augments the deacetylase activity of Sirt3, promoting both OXPHOS and mitochondrial fusion. Mechanistically, SENP1 activates Sirt3 deacetylase activity in T cell mitochondria, leading to reduction of the acetylation of mitochondrial metalloprotease YME1L1. Consequently, deacetylation of YME1L1 suppresses its activity on OPA1 cleavage to facilitate mitochondrial fusion, which results in T cell survival and promotes T cell memory development. We also show that the glycolytic intermediate fructose-1,6-bisphosphate (FBP) as a negative regulator suppresses AMPK-mediated activation of the SENP1-Sirt3 axis and reduces memory development. Moreover, glucose limitation reduces FBP production and activates AMPK during T cell memory development. These data show that glucose limitation activates AMPK and the subsequent SENP1-Sirt3 signalling for T cell memory development.

Indexed as

Immunologic MemoryAcetylationAllograftsAMP-Activated Protein KinasesAnimalsATPases Associated with Diverse Cellular ActivitiesCD8-Positive T-LymphocytesCell Line, TumorCell SurvivalColonic NeoplasmsCysteine EndopeptidasesFructosediphosphatesGlucoseGTP PhosphohydrolasesMetabolomicsMetalloendopeptidasesAMP-Activated Protein KinasesATPases Associated with Diverse Cellular ActivitiesCysteine Endopeptidasesfructose-1,6-diphosphateFructosediphosphatesGlucoseGTP PhosphohydrolasesMetalloendopeptidasesMitochondrial ProteinsOpa1 protein, mouseSenp1 protein, mouseSirtuin 3YME1L1 protein, human

Identifiers

PMID34272364
PMCPMC8285428
OpenAlexW3182725146

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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.