Evidence map›Paper›PMID 37704618›Full record

ArticleCell death discovery2023

NRP1 transduces mechanical stress inhibition via LATS1/YAP in hypertrophic scars.

Mengzhi Li, Peng Wang, Jingting Li, Fei Zhou, Shixin Huang, Shaohai Qi, Bin Shu

Open access · goldAbstract read
In one paragraph

Article in Cell death discovery, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

10 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. The Role of Biomechanical Forces in the Formation and Treatment of Pathological Scars.Clinical, cosmetic and investigational dermatology · 2024
    Review
  10. 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

7 authors at 1 institution in 1 country.

Mengzhi LiDepartment of Burns, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Peng WangDepartment of Burns, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Jingting LiDepartment of Institute of Precision Medicine, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Fei ZhouDepartment of Burns, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Shixin HuangDepartment of Burns, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Shaohai Qi *Department of Burns, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China. qishaohaigzburns@163.com.ORCID http://orcid.org/0000-0001-5962-4203
Bin Shu *Department of Burns, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China. shubin@mail.sysu.edu.cn.ORCID http://orcid.org/0000-0002-7623-4941
Sun Yat-sen University · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) NSFC: 81971833National Natural Science Foundation of China (National Science Foundation of China) NSFC: 81971884National Natural Science Foundation of China (National Science Foundation of China) NSFC: 82172207Natural Science Foundation of Guangdong Province (Guangdong Natural Science Foundation) 2021A1515011806
6 · The paper itself

Abstract

Hypertrophic scar (HS) is an abnormal fibrous hyperplasia of the skin caused by excessive tissue repair in response to skin burns and trauma, which restricts physical function and impairs patients' quality of life. Numerous studies have shown that pressure garment therapy (PGT) is an effective treatment for preventing hypertrophic scars. Herein, we found that mechanical stress stimulates the neuropilin 1 (NRP1) expression through screening GSE165027, GSE137210, and GSE120194 from Gene Expression Omnibus (GEO) database and bioinformatics analysis. We verified this stimulation in the human hypertrophic scar, pressure culture cell model, and rat tail-scar model. Mechanical compression increased LATS1 and pYAP enrichment, thus repressing the expression of YAP. Functionally, the knockdown of NRP1 promoted the expression of LATS1, thus decreasing the expression of YAP and inhibiting endothelial cell proliferation. Furthermore, co-immunoprecipitation analysis confirmed that NRP1 binds to YAP, and mechanical compression disrupted this binding, which resulted in the promotion of YAP relocation to nuclear. In conclusion, our results indicated that NRP1 transduces mechanical force inhibition by inhibiting YAP expression. Mechanical pressure can release YAP bound to NRP1, which explains the phenomenon that mechanical stress increases YAP in the nucleus. Strategies targeting NRP1 may promote compression therapy with optimal and comfortable pressures.

Identifiers

PMID37704618
PMCPMC10499927
OpenAlexW4386709718

What OpenQuestion holds

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LicenceCC BY
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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.