Evidence map›Paper›PMID 36855912›Full record

ArticleEMBO molecular medicine2023

Metabolic rewiring in keratinocytes by miR-31-5p identifies therapeutic intervention for psoriasis.

Mao-Jie Wang, Huan-Jie Huang, Yong-Yue Xu, Harmjan Vos, Can Gulersonmez, Edwin Stigter, Johan Gerritsen, Marc Pages Gallego, Robert van Es, Li Li and 5 more

Open access · goldAbstract read
In one paragraph

Article in EMBO molecular medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

15 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Nomilin Rewires mTOR-Driven Immunometabolism via DDIT4 to Restrain Psoriasis.International journal of biological sciences · 2026
    Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Signaling pathways and targeted therapies for psoriasis.Signal transduction and targeted therapy · 2023
    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

15 authors at 2 institutions in 2 countries.

Mao-Jie WangThe Second Affiliated Hospital, Guangzhou University of Chinese Medicine (Guangdong Provincial Hospital of Chinese Medicine), Guangzhou, China.ORCID 0000-0003-1417-416X
Huan-Jie HuangThe Second Affiliated Hospital, Guangzhou University of Chinese Medicine (Guangdong Provincial Hospital of Chinese Medicine), Guangzhou, China.ORCID 0000-0002-1952-0247
Yong-Yue XuThe Second Affiliated Hospital, Guangzhou University of Chinese Medicine (Guangdong Provincial Hospital of Chinese Medicine), Guangzhou, China.
Harmjan VosOncode Institute and Molecular Cancer Research, Center for Molecular Medicine, University Medical Center Utrecht, Utrecht, The Netherlands.ORCID 0000-0002-4696-6068
Can GulersonmezOncode Institute and Molecular Cancer Research, Center for Molecular Medicine, University Medical Center Utrecht, Utrecht, The Netherlands.
Edwin StigterOncode Institute and Molecular Cancer Research, Center for Molecular Medicine, University Medical Center Utrecht, Utrecht, The Netherlands.ORCID 0000-0001-5970-4668
Johan GerritsenMetabolic Diagnostics, Department of Biomedical Genetics, Centre for Molecular Medicine, University Medical Centre Utrecht, Utrecht, The Netherlands.
Marc Pages GallegoOncode Institute and Department of Genetics, Center for Molecular Medicine, University Medical Center Utrecht, Utrecht, The Netherlands.ORCID 0000-0001-8888-5699
Robert van EsOncode Institute and Molecular Cancer Research, Center for Molecular Medicine, University Medical Center Utrecht, Utrecht, The Netherlands.ORCID 0000-0002-8299-3813
Li LiThe Second Affiliated Hospital, Guangzhou University of Chinese Medicine (Guangdong Provincial Hospital of Chinese Medicine), Guangzhou, China.
Hao DengThe Second Affiliated Hospital, Guangzhou University of Chinese Medicine (Guangdong Provincial Hospital of Chinese Medicine), Guangzhou, China.ORCID 0000-0002-6417-6406
Lin HanThe Second Affiliated Hospital, Guangzhou University of Chinese Medicine (Guangdong Provincial Hospital of Chinese Medicine), Guangzhou, China.
Run-Yue HuangThe Second Affiliated Hospital, Guangzhou University of Chinese Medicine (Guangdong Provincial Hospital of Chinese Medicine), Guangzhou, China.ORCID 0000-0003-1532-1766
Chuan-Jian LuThe Second Affiliated Hospital, Guangzhou University of Chinese Medicine (Guangdong Provincial Hospital of Chinese Medicine), Guangzhou, China.ORCID 0000-0001-6531-0702
Boudewijn Mt BurgeringOncode Institute and Molecular Cancer Research, Center for Molecular Medicine, University Medical Center Utrecht, Utrecht, The Netherlands.ORCID 0000-0002-4044-9596
Guangzhou University of Chinese Medicine · CNUniversity Medical Center Utrecht · NL

Funding

Guangdong Provincial Hospiotal of Chinse Medicine YN2019HL01Guangdong Provincial Hospiotal of Chinse Medicine YN2019HL02Guangdong Provincial Hospiotal of Chinse Medicine YN2019HL03Guangdong Provincial Hospiotal of Chinse Medicine YN2019QJ09National Natural Science Foundation of China (NSFC) 81873302Oncode InstituteThe 2020 Guangdong Provincial Science and Technology Innovation Strategy Special Fund 2020B1212030006
6 · The paper itself

Abstract

Besides genetic alterations, the cellular environment also determines disease onset and progression. When different cell types contribute to disease outcome, this imposes environmental challenges as different cell types likely differ in their extracellular dependencies. Hsa-microRNA-31-5p (miR-31) is highly expressed in keratinocytes of psoriatic skin, and we show that expression in keratinocytes is induced by limited glucose availability and enables increased survival under limiting glucose conditions by increasing glutamine metabolism. In addition, miR-31 expression results in not only secretion of specific metabolites (aspartate and glutamate) but also secretion of immunomodulatory factors. We show that this miR-31-induced secretory phenotype is sufficient to induce Th17 cell differentiation, a hallmark of psoriasis. Inhibitors of miR31-induced metabolic rewiring and metabolic crosstalk with immune cells alleviate psoriasis pathology in a mouse model of psoriasis. Together our data illustrate an emerging concept of metabolic interaction across cell compartments that characterizes disease development, which can be employed to design effective treatment options for disease, as shown here for psoriasis.

Indexed as

MicroRNAsPsoriasisAnimalsCell DifferentiationCell ProliferationKeratinocytesMiceSkinMicroRNAsglutaminolysismetabolism reprogrammingmiR-31psoriasisT helper 17 cells

Identifiers

PMID36855912
PMCPMC10086589
OpenAlexW4322719593

What OpenQuestion holds

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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.