Evidence map›Paper›PMID 37151254›Full record

ArticleIndian journal of dermatology

Heparanase Contributes to Psoriatic Lesions Through Crosstalk with IL-17 Pathway.

Chengyao Zhu, Yunqin Ren, Hongliang Yao, Bo Feng, Lunfei Liu, Min Zheng

Open access · diamondAbstract read
In one paragraph

Article in Indian journal of dermatology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.7field-weighted citation impact, top 28% 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

2 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. The Pathophysiological Functions of Heparanases: From Evolution, Structural and Tissue-Specific Perspectives.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    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

6 authors at 1 institution in 1 country.

Chengyao ZhuDepartment of Dermatology, The Fourth Affiliated Hospital of Zhejiang University School of Medicine, Yiwu, China.
Yunqin RenDepartment of Dermatology, The Children's Hospital of Zhejiang University School of Medicine, Hangzhou, China.
Hongliang YaoDepartment of Dermatology, The Fourth Affiliated Hospital of Zhejiang University School of Medicine, Yiwu, China.
Bo FengDepartment of Dermatology, The Fourth Affiliated Hospital of Zhejiang University School of Medicine, Yiwu, China.
Lunfei LiuDepartment of Dermatology, The Fourth Affiliated Hospital of Zhejiang University School of Medicine, Yiwu, China.
Min ZhengDepartment of Dermatology, The Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, China.
Second Affiliated Hospital of Zhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Psoriasis is a chronic inflammatory disease that is considered by a network of immunocytes and cytokines. Among all, Th17 cells-derived IL-17 is a critical driving factor in the pathogenesis of psoriasis. Recently, disruption of the extracellular matrix was found to be related to psoriasis progression. In the present study, we aimed to investigate the role of heparanase (HPSE) in psoriasis and the crosstalk with the IL-17 signalling pathway. Skin tissues from non-affected areas and psoriatic lesion areas before and after 12 weeks of IL-17 monoclonal antibody treatment of 30 psoriasis patients were collected. HaCaT cells were treated with different concentrations of IL-17 antibody, and HPSE in cells and medium were measured with Western blotting assay as well as enzyme-linked immunosorbent assay (ELISA). In the imiquimod (IMQ)-induced psoriasis model, IL-17 protein and mRNA expression levels were measured, and changes in the proportion of Th17 cells were detected via flow cytometry. Our data showed that HPSE is upregulated in lesion tissues isolated from psoriasis patients, and was inhibited by anti-IL-17 treatment. In cutaneous cells and IMQ-induced psoriasis model, IL-17 promoted the synthesis of HPSE. Inversely, HPSE was also found to increase the percentage of Th17 cells derived from CD4+ T cells. Finally, we found that the combined treatments of HPSE inhibitor and IL-17 monoclonal antibody produced therapeutic effects on IMQ-induced psoriasis model. Our findings revealed the new role of HPSE in the pathogenesis of psoriasis and also provided a target for combined treatment of psoriasis.

Indexed as

HeparanaseIL-17psoriasisTh17 cells

Identifiers

PMID37151254
PMCPMC10162766
OpenAlexW4375856626

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.