Evidence map›Paper›PMID 31140657›Full record

ReviewExperimental dermatology2019

Contribution of fibroblasts to tunnel formation and inflammation in hidradenitis suppurativa/ acne inversa.

John W Frew, Kristina Navrazhina, Meaghan Marohn, Pei-Ju C Lu, James G Krueger

Open access · bronzeAbstract readReview
In one paragraph

Review in Experimental dermatology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
5.7field-weighted citation impact, top 4% 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

27 citing papers in PubMed, 56 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Review
  5. Hidradenitis Suppurativa Tunnels: Unveiling a Unique Disease Entity.JID innovations : skin science from molecules to population health · 2025
    Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Epigenetic switch reshapes epithelial progenitor cell signatures and drives inflammatory pathogenesis in hidradenitis suppurativa.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  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

5 authors at 2 institutions in 1 country.

John W FrewLaboratory of Investigative Dermatology, Rockefeller University, New York, New York.ORCID 0000-0001-5042-3632
Kristina NavrazhinaLaboratory of Investigative Dermatology, Rockefeller University, New York, New York.ORCID 0000-0003-1405-2955
Meaghan MarohnThe Hansjörg Wyss Department of Plastic Surgery, Department of Cell Biology, New York University, New York, New York.
Pei-Ju C LuThe Hansjörg Wyss Department of Plastic Surgery, Department of Cell Biology, New York University, New York, New York.
James G KruegerLaboratory of Investigative Dermatology, Rockefeller University, New York, New York.
Rockefeller University · USNew York University · US

Funding

Weill Cornell/Rockefeller/Sloan-Kettering MST ProgramT32GM007739 · NIGMS · WEILL MEDICAL COLL OF CORNELL UNIV · PI HSU, KATHARINE C · 1985 to 2023
$51.1M
Developing, Demonstrating, and Disseminating Innovative Programs to Achieve Translational SuccessUL1TR001866 · NCATS · ROCKEFELLER UNIVERSITY · PI COLLER, BARRY, KRUEGER, JAMES G · 2016 to 2025
$40.6M
NCATS NIH HHS UL1 TR001866NIGMS NIH HHS T32 GM007739
6 · The paper itself

Abstract

The precise pathogenic mechanisms in the development, persistence and worsening of hidradenitis suppurativa (HS) remain ill-defined. This chronic inflammatory dermatosis displays a strong Th1 and Th17 inflammatory signature with elevated levels of TNF-α, IL-1β, IL-17 and IFNγ in lesional and perilesional tissue. HS significantly differs to other chronic inflammatory dermatoses due to the development of hypertrophic scarring and dermal tunnels. The development of scarring and tunnels suggests that fibroblastic stromal cells (including myofibroblasts, fibroblasts, pericytes etc) may be involved in the development and progression of disease. Heterogeneous populations of fibroblasts have been identified in other inflammatory disorders and malignancy which contribute to inflammation and present novel therapeutic targets for fibrotic disorders. Findings in HS are consistent with these fibroblast subpopulations and may contribute to tunnel formation, aggressive squamous cell carcinoma and the phenotypic presentation of familial HS variants. We describe the existing knowledge regarding these mechanistic pathways and methods to confirm their involvement in the pathogenesis of HS.

Indexed as

Amyloid Precursor Protein SecretasesFibroblastsHidradenitis SuppurativaHumansInflammatory Bowel DiseasesMatrix MetalloproteinasesMesenchymal Stem CellsNeoplasmsAmyloid Precursor Protein SecretasesMatrix Metalloproteinasesacne inversafibroblastshidradenitis suppurativapathogenesisscarring

Identifiers

PMID31140657
PMCPMC6663622
OpenAlexW2947352805

What Socratic holds

Textmetadata
LicenceTDM
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 Socratic graph.