Evidence map›Paper›PMID 39240413›Full record

ArticleArchives of dermatological research2024

Pilot study of the role of ferroptosis in abnormal biological behaviour of keratinocytes in psoriasis vulgaris.

Ningling Wu, Qian Hu, Zhibing Fu, Xiaoliang Tong, Lihua Gao, Lina Tan, Siyu Yan, Dan Wang, Jinrong Zeng, Jianyun Lu and 1 more

Abstract read
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In one paragraph

Article in Archives of dermatological research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
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

5 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Programmed cell death of keratinocytes: an active driver in psoriasis.Apoptosis : an international journal on programmed cell death · 2026
    Review
  5. Article
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.

Ningling Wu *Department of Dermatology, Third Xiangya Hospital, Central South University, Changsha, 410013, Hunan, China.ORCID http://orcid.org/0000-0002-9802-737X
Qian Hu *Department of Dermatology, Changsha Fourth Hospital, Changsha, 410006, Hunan, China.
Zhibing FuDepartment of Dermatology, Third Xiangya Hospital, Central South University, Changsha, 410013, Hunan, China.
Xiaoliang TongDepartment of Dermatology, Third Xiangya Hospital, Central South University, Changsha, 410013, Hunan, China.
Lihua GaoDepartment of Dermatology, Third Xiangya Hospital, Central South University, Changsha, 410013, Hunan, China.
Lina TanDepartment of Dermatology, Third Xiangya Hospital, Central South University, Changsha, 410013, Hunan, China.
Siyu YanDepartment of Dermatology, Third Xiangya Hospital, Central South University, Changsha, 410013, Hunan, China.
Dan WangDepartment of Dermatology, Third Xiangya Hospital, Central South University, Changsha, 410013, Hunan, China.
Jinrong ZengDepartment of Dermatology, Third Xiangya Hospital, Central South University, Changsha, 410013, Hunan, China.
Jianyun LuDepartment of Dermatology, Third Xiangya Hospital, Central South University, Changsha, 410013, Hunan, China.
Wenchuan LiDepartment of Dermatology, Third Xiangya Hospital, Central South University, Changsha, 410013, Hunan, China. LeeVinson96@163.com.

Funding

Hunan Provincial Natural Science Outstanding Youth Fund No.2023JJ20089the Research Project of the Hunan Provincial Health Commission No.202204124175
6 · The paper itself

Abstract

backgroundAbnormal biological behaviour of keratinocytes (KCs) is a critical pathophysiological manifestation of psoriasis. Ferroptosis is programmed cell death induced by the accumulation of lipid reactive oxygen species (ROS) in the presence of increased intracellular iron ions or inhibition of GPX4.

objectivesThe purpose of this study was to investigate the effects of ferroptosis on the biological behaviour of Keratinocytes (KCs) in psoriasis vulgaris and its possible regulatory mechanisms in clinical samples, cells, and mouse models.

methodsWe first examined the differences in the expression of GPX4 and 4-HNE between psoriasis and normal human lesions. And detected KRT6, FLG, and inflammatory cytokines after inducing ferroptosis in animal and cell models by RT-qPCR, Western blot, immunohistochemistry, and flow cytometry.

resultsWe found that GPX4 was decreased and that the oxidation product 4-hydroxy-2-nonenal (HNE) was increased in the skin lesions of patients with psoriasis vulgaris. The expression level of GPX4 correlates with the severity of skin lesions. Moreover, inducing ferroptosis promoted the expression of FLG and reduced the expression of KRT6 and inflammatory cytokines in vitro, and alleviated the phenotype of skin lesions in vivo. LIMITATIONS: Our study has limitations, notably small sample size. Larger clinical trials are necessary to investigate the association between ferroptosis and disease progression further. More research is necessary to explore how the ferroptosis inducer RSL3 regulates the abnormal biological behaviour of KCs at both cellular and animal levels and establish ferroptosis inhibitors as controls.

conclusionsThis study confirms the existence of ferroptosis in psoriatic lesions, which may be inversely correlated with disease severity. The ferroptosis inducer RSL3 ameliorated psoriatic symptoms by improving the abnormal biological behaviour of KCs.

Indexed as

Disease Models, AnimalFerroptosisKeratinocytesPhospholipid Hydroperoxide Glutathione PeroxidasePsoriasisAdultAldehydesAnimalsCarbolinesCytokinesFemaleHumansKeratin-6MaleMiceMiddle Aged4-hydroxy-2-nonenalAldehydesCarbolinesCytokinesKeratin-6Phospholipid Hydroperoxide Glutathione PeroxidaseReactive Oxygen SpeciesResorcinolsRSL3 compoundAbnormal biological behavioursFerroptosisGPX4KeratinocytesPsoriasis vulgaris

Identifiers

PMID39240413

What OpenQuestion holds

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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.