Evidence map›Paper›PMID 34733164›Full record

ArticleFrontiers in pharmacology2021

Pyruvate Kinase M2 Mediates Glycolysis Contributes to Psoriasis by Promoting Keratinocyte Proliferation.

Yun-Zi Liu, Ming-Yuan Xu, Xiao-Yu Dai, Lang Yan, Lei Li, Rui-Zhen Zhu, Li-Jun Ren, Ji-Qian-Zhu Zhang, Xiao-Fang Zhang, Jin-Feng Li and 6 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in pharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

29 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
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  4. Article
  5. Article
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  10. Sensory nerve-secreted factors regulate basal keratinocyte functionIntegrative organismal biology (Oxford, England) · 2025
    Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Signaling pathways and targeted therapies for psoriasis.Signal transduction and targeted therapy · 2023
    Review
  16. Review
  17. Article
  18. Dry eye disease in mice activates adaptive corneal epithelial regeneration distinct from constitutive renewal in homeostasis.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  19. Article
  20. 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

16 authors at 4 institutions in 1 country.

Yun-Zi LiuDepartment of Health Toxicology, Faculty of Naval Medicine, Second Military Medical University, Shanghai, China.
Ming-Yuan XuDepartment of Dermatopathology, Shanghai Skin Disease Hospital Affiliated to Tongji University, Shanghai, China.
Xiao-Yu DaiDepartment of Health Toxicology, Faculty of Naval Medicine, Second Military Medical University, Shanghai, China.
Lang YanDepartment of Health Toxicology, Faculty of Naval Medicine, Second Military Medical University, Shanghai, China.
Lei LiThe Second Naval Hospital of the Southern Theater of the Chinese People's Liberation Army, Hainan, China.
Rui-Zhen ZhuDepartment of Dermatopathology, Shanghai Skin Disease Hospital Affiliated to Tongji University, Shanghai, China.
Li-Jun RenDepartment of Health Toxicology, Faculty of Naval Medicine, Second Military Medical University, Shanghai, China.
Ji-Qian-Zhu ZhangDepartment of Health Toxicology, Faculty of Naval Medicine, Second Military Medical University, Shanghai, China.
Xiao-Fang ZhangDepartment of Health Toxicology, Faculty of Naval Medicine, Second Military Medical University, Shanghai, China.
Jin-Feng LiDepartment of Health Toxicology, Faculty of Naval Medicine, Second Military Medical University, Shanghai, China.
Yi-Jun TianDepartment of Health Toxicology, Faculty of Naval Medicine, Second Military Medical University, Shanghai, China.
Wen-Jing ShiDepartment of Health Toxicology, Faculty of Naval Medicine, Second Military Medical University, Shanghai, China.
Ye-Qiang LiuDepartment of Dermatopathology, Shanghai Skin Disease Hospital Affiliated to Tongji University, Shanghai, China.
Chun-Lei JiangLaboratory of Stress Medicine, Faculty of Psychology and Mental Health, Second Military Medical University, Shanghai, China.
Jiang-Bo ZhuDepartment of Health Toxicology, Faculty of Naval Medicine, Second Military Medical University, Shanghai, China.
Ji-Kuai ChenDepartment of Health Toxicology, Faculty of Naval Medicine, Second Military Medical University, Shanghai, China.
Second Military Medical University · CNTongji University · CNChinese People's Liberation Army · CNShanghai Skin Disease Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Psoriasis is characterized by keratinocyte proliferation and immune cell infiltration. M2 isoform of pyruvate kinase (PKM2) was reported to have an important role in cell proliferation, which is a rate-limiting enzyme that regulates the final step of glycolysis. However, how PKM2 regulates cell metabolism and proliferation in psoriatic keratinocytes is still poorly understood. Interestingly, we found that PKM2 was highly expressed in psoriatic epidermis from patients and mouse models. PKM2 overexpression promoted keratinocyte glycolytic metabolism while knockdown inhibited keratinocyte proliferation and glycolysis. Mice lacking PKM2 specifically in keratinocytes, pharmacological inhibition of PKM2 or glycolysis inhibited keratinocyte proliferation and showed obvious remission in an imiquimod-induced psoriatic mouse model. Moreover, the inhibitor of the EGF-receptor blocked EGF-stimulated PKM2 expression and glycolysis in keratinocytes. We identify PKM2 as an upregulated gene in psoriasis. PKM2 is essential in keratinocyte over-proliferation and may represent a therapeutic target for psoriasis.

Indexed as

glycolysiskeratinocytepsoriasispyruvate kinase M2shikonin

Identifiers

PMID34733164
PMCPMC8558409
OpenAlexW3206795571

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.