Evidence map›Paper›PMID 37215989›Full record

ArticleInternational journal of biological sciences2023

Enhancement of Zyxin Promotes Skin Fibrosis by Regulating FAK/PI3K/AKT and TGF-β Signaling Pathways via Integrins.

Yan Huang, Han Zhao, Yuting Zhang, Yulong Tang, Xiangguang Shi, Shuai Jiang, Weilin Pu, Jing Liu, Yanyun Ma, Juiming Lin and 5 more

Open access · goldAbstract read
In one paragraph

Article in International journal of biological sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
10.2field-weighted citation impact, top 1% 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

36 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
  2. Scleral Postn Drives Myopia via Promoting Myofibroblast Transdifferentiation.Investigative ophthalmology & visual science · 2026
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  13. Stem cell therapy targets THBS1 to reverse endometrial fibrosis.Frontiers in cell and developmental biology · 2026
    Article
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  19. Article
  20. Systemic sclerosis, main culprits and involved signaling pathways.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 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

15 authors at 3 institutions in 1 country.

Yan HuangState Key Laboratory of Genetic Engineering, Collaborative Innovation Center for Genetics and Development, School of Life Sciences, and Human Phenome Institute, Fudan University, Shanghai, China.
Han ZhaoState Key Laboratory of Genetic Engineering, Collaborative Innovation Center for Genetics and Development, School of Life Sciences, and Human Phenome Institute, Fudan University, Shanghai, China.
Yuting ZhangState Key Laboratory of Genetic Engineering, Collaborative Innovation Center for Genetics and Development, School of Life Sciences, and Human Phenome Institute, Fudan University, Shanghai, China.
Yulong TangState Key Laboratory of Genetic Engineering, Collaborative Innovation Center for Genetics and Development, School of Life Sciences, and Human Phenome Institute, Fudan University, Shanghai, China.
Xiangguang ShiDivision of Dermatology, Huashan Hospital, Fudan University, Shanghai Institute of Dermatology Shanghai, China.
Shuai JiangState Key Laboratory of Genetic Engineering, Collaborative Innovation Center for Genetics and Development, School of Life Sciences, and Human Phenome Institute, Fudan University, Shanghai, China.
Weilin PuState Key Laboratory of Genetic Engineering, Collaborative Innovation Center for Genetics and Development, School of Life Sciences, and Human Phenome Institute, Fudan University, Shanghai, China.
Jing LiuState Key Laboratory of Genetic Engineering, Collaborative Innovation Center for Genetics and Development, School of Life Sciences, and Human Phenome Institute, Fudan University, Shanghai, China.
Yanyun MaInstitute for Six-sector Economy, Fudan University, Shanghai, China.
Juiming LinDivision of Dermatology, Huashan Hospital, Fudan University, Shanghai Institute of Dermatology Shanghai, China.
Jinran LinDivision of Dermatology, Huashan Hospital, Fudan University, Shanghai Institute of Dermatology Shanghai, China.
Wenyu WuDivision of Dermatology, Huashan Hospital, Fudan University, Shanghai Institute of Dermatology Shanghai, China.
Yiyi GongDivision of Dermatology, Huashan Hospital, Fudan University, Shanghai Institute of Dermatology Shanghai, China.
Jiucun WangState Key Laboratory of Genetic Engineering, Collaborative Innovation Center for Genetics and Development, School of Life Sciences, and Human Phenome Institute, Fudan University, Shanghai, China.
Qingmei LiuDivision of Dermatology, Huashan Hospital, Fudan University, Shanghai Institute of Dermatology Shanghai, China.
Fudan University · CNState Key Laboratory of Genetic EngineeringJingzhou Central Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Skin fibrosis is a common pathological manifestation in systemic sclerosis (SSc), keloid, and localized scleroderma (LS) characterized by fibroblast activation and excessive extracellular matrix (ECM) deposition. However, few effective drugs are available to treat skin fibrosis due to its unclear mechanisms. In our study, we reanalyzed skin RNA-sequencing data of Caucasian, African, and Hispanic SSc patients from the Gene Expression Omnibus (GEO) database. We found that the focal adhesion pathway was up-regulated and Zyxin appeared to be the primary focal adhesion protein involved in skin fibrosis, and we further verified its expression in Chinese skin tissues of several fibrotic diseases, including SSc, keloid, and LS. Moreover, we found Zyxin inhibition could significantly alleviate skin fibrosis using Zyxin knock-down and knock-out mice, nude mouse model and skin explants of human keloid. Double immunofluorescence staining showed that Zyxin was highly expressed in fibroblasts. Further analysis revealed pro-fibrotic gene expression and collagen production increased in Zyxin over-expressed fibroblasts, and decreased in Zyxin interfered SSc fibroblasts. In addition, transcriptome and cell culture analyses revealed Zyxin inhibition could effectively attenuate skin fibrosis by regulating the FAK/PI3K/AKT and TGF-β signaling pathways via integrins. These results suggest Zyxin appears a potential new therapeutic target for skin fibrosis.

Indexed as

KeloidScleroderma, SystemicZyxinAnimalsFibroblastsFibrosisHumansIntegrinsMicePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionSkinTransforming Growth Factor betaIntegrinsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTransforming Growth Factor betaZyxinZYX protein, humanECMFocal adhesionIntegrinsSkin fibrosisSystemic sclerosisZyxin

Identifiers

PMID37215989
PMCPMC10197900
OpenAlexW4372047048

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.