Evidence map›Paper›PMID 40108109›Full record

ArticleCell death & disease2025

YAP1 facilitates the pathogenesis of psoriasis via modulating keratinocyte proliferation and inflammation.

Cong Huang, Wenting Li, Changbing Shen, Bin Jiang, Kaoyuan Zhang, Xiahong Li, Weilong Zhong, Zizhuo Li, Zhenzhen Chen, Chaofeng Chen and 5 more

Abstract read
In one paragraph

Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing 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

13 citing papers in PubMed.

  1. Article
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  8. Regulatory role of POSTN in keloid pathogenesis.Molecular medicine reports · 2025
    Article
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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

15 authors.

Cong Huang *Department of Dermatology, Skin Research Institute of Peking University Shenzhen Hospital, Peking University Shenzhen Hospital, Shenzhen Key Laboratory for Translational Medicine of Dermatology, Shenzhen Peking University - The Hong Kong University of Science and Technology Medical Center, Shenzhen, China. conghuangphd1988@163.com.ORCID http://orcid.org/0000-0002-6064-8488
Wenting Li *Department of Dermatology, Skin Research Institute of Peking University Shenzhen Hospital, Peking University Shenzhen Hospital, Shenzhen Key Laboratory for Translational Medicine of Dermatology, Shenzhen Peking University - The Hong Kong University of Science and Technology Medical Center, Shenzhen, China.
Changbing Shen *Department of Dermatology, Skin Research Institute of Peking University Shenzhen Hospital, Peking University Shenzhen Hospital, Shenzhen Key Laboratory for Translational Medicine of Dermatology, Shenzhen Peking University - The Hong Kong University of Science and Technology Medical Center, Shenzhen, China.
Bin Jiang *Department of Dermatology, Skin Research Institute of Peking University Shenzhen Hospital, Peking University Shenzhen Hospital, Shenzhen Key Laboratory for Translational Medicine of Dermatology, Shenzhen Peking University - The Hong Kong University of Science and Technology Medical Center, Shenzhen, China.
Kaoyuan ZhangDepartment of Dermatology, Skin Research Institute of Peking University Shenzhen Hospital, Peking University Shenzhen Hospital, Shenzhen Key Laboratory for Translational Medicine of Dermatology, Shenzhen Peking University - The Hong Kong University of Science and Technology Medical Center, Shenzhen, China.
Xiahong LiDepartment of Dermatology, Skin Research Institute of Peking University Shenzhen Hospital, Peking University Shenzhen Hospital, Shenzhen Key Laboratory for Translational Medicine of Dermatology, Shenzhen Peking University - The Hong Kong University of Science and Technology Medical Center, Shenzhen, China.
Weilong ZhongDepartment of Dermatology, Skin Research Institute of Peking University Shenzhen Hospital, Peking University Shenzhen Hospital, Shenzhen Key Laboratory for Translational Medicine of Dermatology, Shenzhen Peking University - The Hong Kong University of Science and Technology Medical Center, Shenzhen, China.
Zizhuo LiDepartment of Dermatology, Skin Research Institute of Peking University Shenzhen Hospital, Peking University Shenzhen Hospital, Shenzhen Key Laboratory for Translational Medicine of Dermatology, Shenzhen Peking University - The Hong Kong University of Science and Technology Medical Center, Shenzhen, China.
Zhenzhen ChenDepartment of Dermatology, Skin Research Institute of Peking University Shenzhen Hospital, Peking University Shenzhen Hospital, Shenzhen Key Laboratory for Translational Medicine of Dermatology, Shenzhen Peking University - The Hong Kong University of Science and Technology Medical Center, Shenzhen, China.
Chaofeng ChenDepartment of Dermatology, Skin Research Institute of Peking University Shenzhen Hospital, Peking University Shenzhen Hospital, Shenzhen Key Laboratory for Translational Medicine of Dermatology, Shenzhen Peking University - The Hong Kong University of Science and Technology Medical Center, Shenzhen, China.
Xingling JianDepartment of Dermatology, Skin Research Institute of Peking University Shenzhen Hospital, Peking University Shenzhen Hospital, Shenzhen Key Laboratory for Translational Medicine of Dermatology, Shenzhen Peking University - The Hong Kong University of Science and Technology Medical Center, Shenzhen, China.
Xiaoming LiuDepartment of Dermatology, Skin Research Institute of Peking University Shenzhen Hospital, Peking University Shenzhen Hospital, Shenzhen Key Laboratory for Translational Medicine of Dermatology, Shenzhen Peking University - The Hong Kong University of Science and Technology Medical Center, Shenzhen, China.
Haiyan HuangDepartment of Dermatology, Skin Research Institute of Peking University Shenzhen Hospital, Peking University Shenzhen Hospital, Shenzhen Key Laboratory for Translational Medicine of Dermatology, Shenzhen Peking University - The Hong Kong University of Science and Technology Medical Center, Shenzhen, China.
Lili YangDepartment of Dermatology, Skin Research Institute of Peking University Shenzhen Hospital, Peking University Shenzhen Hospital, Shenzhen Key Laboratory for Translational Medicine of Dermatology, Shenzhen Peking University - The Hong Kong University of Science and Technology Medical Center, Shenzhen, China.
Bo YuDepartment of Dermatology, Skin Research Institute of Peking University Shenzhen Hospital, Peking University Shenzhen Hospital, Shenzhen Key Laboratory for Translational Medicine of Dermatology, Shenzhen Peking University - The Hong Kong University of Science and Technology Medical Center, Shenzhen, China. drboyu_derm@126.com.

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82103726National Natural Science Foundation of China (National Science Foundation of China) 82203900
6 · The paper itself

Abstract

Psoriasis is an autoinflammatory skin disease characterized by the abnormal activation of epidermal keratinocytes. The Hippo-YAP pathway is an evolutionarily conserved pathway that plays important roles in organ size control and tumorigenesis. Recently, accumulating evidence demonstrated that YAP1, the core downstream component of Hippo-YAP pathway, was up-regulated in psoriasis patients, suggesting its possible role in psoriasis development. However, its precise function and mechanism in psoriasis pathogenesis are still not well-clarified. In the present study, we confirmed the up-regulation of YAP1 in psoriasis keratinocytes by measuring its expression in psoriatic patient skins, psoriatic-like cellular model, and IMQ-induced mouse model. Further functional studies showed that YAP1 promoted keratinocyte proliferation and inflammation in vitro. Meanwhile, VP, a selective YAP1 antagonist, inhibited keratinocyte proliferation and inflammatory factor production in a dose-dependent way. Moreover, intradermal injection of si-Yap1 or VP hindered psoriasis development by impeding epidermal hyperplasia and relieving systemic inflammatory response in the IMQ-induced mouse model. Therefore, our findings suggest that YAP1 plays a crucial role in psoriasis pathogenesis through modulating keratinocyte activation and may serve as a novel target for the treatment of psoriasis.

Indexed as

Adaptor Proteins, Signal TransducingInflammationKeratinocytesPsoriasisTranscription FactorsAnimalsCell Cycle ProteinsCell ProliferationDisease Models, AnimalHumansMaleMiceYAP-Signaling ProteinsAdaptor Proteins, Signal TransducingCell Cycle ProteinsTranscription FactorsYAP1 protein, humanYap1 protein, mouseYAP-Signaling Proteins

Identifiers

PMID40108109
PMCPMC11923178

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Registered trials

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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.