Evidence map›Paper›PMID 28700632›Full record

ArticlePloS one2017

Inflammation dependent mTORC1 signaling interferes with the switch from keratinocyte proliferation to differentiation.

Claudia Buerger, Nitesh Shirsath, Victoria Lang, Alina Berard, Sandra Diehl, Roland Kaufmann, Wolf-Henning Boehncke, Peter Wolf

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

51 citing papers in PubMed, 82 citations in OpenAlex.

  1. Review
  2. Phytochemical Profiling and Computational Screening ofPharmaceuticals (Basel, Switzerland) · 2026
    Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. mTORC1 and mTORC2 Levels in Patients with Psoriasis.Dermatology practical & conceptual · 2024
    Article
  10. Article
  11. Article
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  13. Article
  14. Pathogenesis and management ofFrontiers in genetics · 2024
    Review
  15. Article
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  17. Review
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  20. 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

8 authors at 3 institutions in 3 countries.

Claudia BuergerDepartment of Dermatology, Venerology and Allergology, Clinic of the Goethe University, Frankfurt am Main, Germany.ORCID http://orcid.org/0000-0002-7838-197X
Nitesh ShirsathDepartment of Dermatology, Medical University of Graz, Graz, Austria.
Victoria LangDepartment of Dermatology, Venerology and Allergology, Clinic of the Goethe University, Frankfurt am Main, Germany.
Alina BerardDepartment of Dermatology, Venerology and Allergology, Clinic of the Goethe University, Frankfurt am Main, Germany.
Sandra DiehlDepartment of Dermatology, Venerology and Allergology, Clinic of the Goethe University, Frankfurt am Main, Germany.
Roland KaufmannDepartment of Dermatology, Venerology and Allergology, Clinic of the Goethe University, Frankfurt am Main, Germany.
Wolf-Henning BoehnckeDepartment of Dermatology and Venereology, Geneva University Hospital, Geneva, Switzerland.
Peter WolfDepartment of Dermatology, Medical University of Graz, Graz, Austria.
Goethe University Frankfurt · DEMedical University of Graz · ATUniversity of Geneva · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Psoriasis is a frequent and often severe inflammatory skin disease, characterized by altered epidermal homeostasis. Since we found previously that Akt/mTOR signaling is hyperactivated in psoriatic skin, we aimed at elucidating the role of aberrant mTORC1 signaling in this disease. We found that under healthy conditions mTOR signaling was shut off when keratinocytes switch from proliferation to terminal differentiation. Inflammatory cytokines (IL-1β, IL-17A, TNF-α) induced aberrant mTOR activity which led to enhanced proliferation and reduced expression of differentiation markers. Conversely, regular differentiation could be restored if mTORC1 signaling was blocked. In mice, activation of mTOR through the agonist MHY1485 also led to aberrant epidermal organization and involucrin distribution. In summary, these results not only identify mTORC1 as an important signal integrator pivotal for the cells fate to either proliferate or differentiate, but emphasize the role of inflammation-dependent mTOR activation as a psoriatic pathomechanism.

Indexed as

AdolescentAdultAgedAnimalsCell DifferentiationCell LineCell ProliferationFemaleHumansImmunoassayImmunohistochemistryKeratinocytesMaleMechanistic Target of Rapamycin Complex 1MiceMice, Inbred BALB CMechanistic Target of Rapamycin Complex 1Multiprotein ComplexesRNA, Small InterferingTOR Serine-Threonine Kinases

Identifiers

PMID28700632
PMCPMC5507280
OpenAlexW2734333850

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.