Evidence map›Paper›PMID 34645459›Full record

ArticleJournal of neuroinflammation2021

Pyruvate kinase isoform M2 impairs cognition in systemic lupus erythematosus by promoting microglial synaptic pruning via the β-catenin signaling pathway.

Li Lu, Hailin Wang, Xuan Liu, Liping Tan, Xiaoyue Qiao, Jiali Ni, Yang Sun, Jun Liang, Yayi Hou, Huan Dou

Open access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
4.2field-weighted citation impact, top 5% 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

31 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. PKM2: A gatekeeper in macrophage metabolic reprogramming.Journal of pharmaceutical analysis · 2026
    Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. The MRL Model: A Valuable Tool in Studies of Autoimmunity-Brain Interactions.Methods in molecular biology (Clifton, N.J.) · 2025
    Review
  18. Review
  19. Article
  20. Tetramerization of PKM2 Alleviates Traumatic Brain Injury by Ameliorating Mitochondrial Damage in Microglia.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2024
    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

10 authors at 3 institutions in 1 country.

Li Lu *The State Key Laboratory of Pharmaceutical Biotechnology, Division of Immunology, Medical School, Nanjing University, Nanjing, 210093, People's Republic of China.
Hailin Wang *The State Key Laboratory of Pharmaceutical Biotechnology, Division of Immunology, Medical School, Nanjing University, Nanjing, 210093, People's Republic of China.
Xuan LiuThe State Key Laboratory of Pharmaceutical Biotechnology, Division of Immunology, Medical School, Nanjing University, Nanjing, 210093, People's Republic of China.
Liping TanThe State Key Laboratory of Pharmaceutical Biotechnology, Division of Immunology, Medical School, Nanjing University, Nanjing, 210093, People's Republic of China.
Xiaoyue QiaoThe State Key Laboratory of Pharmaceutical Biotechnology, Division of Immunology, Medical School, Nanjing University, Nanjing, 210093, People's Republic of China.
Jiali NiThe State Key Laboratory of Pharmaceutical Biotechnology, Division of Immunology, Medical School, Nanjing University, Nanjing, 210093, People's Republic of China.
Yang SunThe State Key Laboratory of Pharmaceutical Biotechnology and Collaborative Innovation Center of Chemistry for Life Sciences, School of Life Sciences, Nanjing University, Nanjing, 210023, China. yangsun@nju.edu.cn.
Jun LiangDepartment of Rheumatology and Immunology, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, Nanjing, 210008, People's Republic of China. 13505193169@139.com.
Yayi HouThe State Key Laboratory of Pharmaceutical Biotechnology, Division of Immunology, Medical School, Nanjing University, Nanjing, 210093, People's Republic of China. yayihou@nju.edu.cn.
Huan DouThe State Key Laboratory of Pharmaceutical Biotechnology, Division of Immunology, Medical School, Nanjing University, Nanjing, 210093, People's Republic of China. douhuan@nju.edu.cn.ORCID http://orcid.org/0000-0001-6330-398X
Nanjing University · CNChina Pharmaceutical University · CNNanjing Drum Tower Hospital · CN

Funding

Jiangsu Province key Social and Development R&A Grant BE2019706Jiangsu Province Six Talent Peaks Project 2016-WSN-148Jiangsu Province Six Talent Peaks Project YY-021Jiangsu Provincial Medical Youth Talent QNRC2016005National Natural Science Foundation of China 31872732National Natural Science Foundation of China 32070883Research Project of Jiangsu Province Health Committee H2019060
6 · The paper itself

Abstract

backgroundNeuropsychiatric systemic lupus erythematosus (NPSLE) is a severe complication, which involves pathological damage to the brain and cognitive function. However, its exact mechanism of action still remains unclear. In this study, we explored the role of microglia in the cognitive dysfunction of NPSLE mice. We also analyzed and compared the metabolites in the hippocampal tissues of the lupus model and control mice.

methodsMRL/MpJ-Fas

resultsGlycolysis was elevated in the hippocampus of MRL/lpr lupus mice, accompanied by increased glucose consumption and lactate production. Furthermore, the activation of PKM2 in hippocampal microglia was observed in lupus mice. Cell experiments showed that PKM2 facilitated microglial activation and over-activated microglial phagocytosis via the β-catenin signaling pathway. In vivo, AAV9-shPKM2-treated mice showed decreased microglial activation and reduced neuronal synapses loss by blocking the β-catenin signaling pathway. Furthermore, the cognitive impairment and brain damage of MRL/lpr mice were significantly relieved after microglial PKM2 inhibition.

conclusionThese data indicate that microglial PKM2 have potential to become a novel therapeutic target for treating lupus encephalopathy.

Indexed as

Animalsbeta CateninCell LineCognitive DysfunctionFemaleLupus Erythematosus, SystemicMiceMice, Inbred C57BLMice, Inbred MRL lprMicrogliaNeuronal PlasticityPyruvate KinaseSynapsesWnt Signaling Pathwaybeta CateninCTNNB1 protein, mousePkm protein, mousePyruvate KinaseAerobic glycolysisLC–MS analysisMicrogliaPhagocytosisPyruvate kinase isoform M2Systemic lupus erythematosus encephalopathy

Identifiers

PMID34645459
PMCPMC8513209
OpenAlexW3127945804

What OpenQuestion 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 OpenQuestion graph.