Evidence map›Paper›PMID 33641447›Full record

ArticleExperimental biology and medicine (Maywood, N.J.)2021

Inhibition of phospholipases suppresses progression of psoriasis through modulation of inflammation.

Yunlu Gao, Jiajing Lu, Xunxia Bao, Xuemei Yi, Chen Peng, Wenjuan Chen, Timing Zhen, Yong Shi, Kaichen Xing, Sibo Zhu and 1 more

Open access · greenAbstract read
In one paragraph

Article in Experimental biology and medicine (Maywood, N.J.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.8field-weighted citation impact, top 31% 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

12 citing papers in PubMed, 14 citations in OpenAlex.

  1. Immune Biomarkers of Islet Transplant Rejection Revealed by Synthetic Immunological Niche.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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  11. Mouse Models of Psoriasis: A Comprehensive Review.The Journal of investigative dermatology · 2022
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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

11 authors at 2 institutions in 1 country.

Yunlu GaoDepartment of Dermatology, Shanghai Skin Disease Hospital, Tongji University School of Medicine, Shanghai 200443, China.
Jiajing LuDepartment of Dermatology, Shanghai Skin Disease Hospital, Tongji University School of Medicine, Shanghai 200443, China.ORCID 0000-0002-0827-0596
Xunxia BaoCinoasia Institute, Shanghai 200438, China.ORCID 0000-0002-6085-7319
Xuemei YiDepartment of Dermatology, Shanghai Skin Disease Hospital, Tongji University School of Medicine, Shanghai 200443, China.
Chen PengDepartment of Dermatology, Shanghai Skin Disease Hospital, Tongji University School of Medicine, Shanghai 200443, China.
Wenjuan ChenDepartment of Dermatology, Shanghai Skin Disease Hospital, Tongji University School of Medicine, Shanghai 200443, China.
Timing ZhenCinoasia Institute, Shanghai 200438, China.
Yong ShiCinoasia Institute, Shanghai 200438, China.
Kaichen XingCinoasia Institute, Shanghai 200438, China.
Sibo ZhuSchool of Life Sciences, Fudan University, Shanghai 200438, China.ORCID 0000-0003-4800-8987
Yangfeng DingDepartment of Dermatology, Shanghai Skin Disease Hospital, Tongji University School of Medicine, Shanghai 200443, China.ORCID 0000-0002-4312-0446
Tongji University · CNFudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Abnormal lipid metabolism is regarded as a crucial cause of psoriasis. The specific mechanism of how phospholipase PLA2G4B mediates local immune dysfunction and skin lesions remains unclear. The aim of this study was to explore the mechanisms of anti-psoriasis and immune suppression effect by inhibiting PLA2G4B in psoriasis progression. We successfully transfected si-PLA2G4B in a murine keratinocyte cell-line PAM212 to verify the effect of progression by PLA2G4B. The Imiquimod psoriasis mouse model was then successfully constructed, followed by emulsion wrapped PLA2G4B-siRNA applied to the skin lesions. The phenotype, pathology, immunofluorescence staining of PLA2G4B, IL17, CD3, and CD1b, and bulk transcriptome analysis were performed to decipher the effect and mechanism of si-PLA2G4B. Interfering with PLA2G4B significantly inhibited the proliferation and migration of PAM212. The interference of PLA2G4B

Indexed as

AnimalsAntigens, CD1Cell LineDisease Models, AnimalGene Expression RegulationGroup IV Phospholipases A2HumansImiquimodInflammationInterleukin-17KeratinocytesMaleMiceMice, Inbred BALB CPsoriasisRNA, Small InterferingAntigens, CD1CD1b antigenGroup IV Phospholipases A2Il17a protein, mouseImiquimodInterleukin-17Pla2g4b protein, mouseRNA, Small Interferinginflammatory factorslipid metabolism disordermedicinePLA2G4BPsoriasistranscriptome

Identifiers

PMID33641447
PMCPMC8371307
OpenAlexW3135646089

What OpenQuestion holds

Textmetadata
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.