Evidence map›Paper›PMID 37780385›Full record

ArticlePeerJ2023

TLR7 promotes skin inflammation via activating NFκB-mTORC1 axis in rosacea.

Yaqun Huang, Da Liu, Mengting Chen, San Xu, Qinqin Peng, Yan Zhu, Juan Long, Tangxiele Liu, Zhili Deng, Hongfu Xie and 3 more

Open access · goldAbstract read
In one paragraph

Article in PeerJ, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
3.7field-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, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.

  1. Molecular Mechanisms in the Etiopathology of Rosacea-Systematic Review.International journal of molecular sciences · 2025
    Pooled it
  2. Epithelial-Dermal Immune Memory: TrackingInternational journal of molecular sciences · 2026
    Review
  3. Review
  4. Sex Bias in Autoimmunity: New Findings and New Opportunities.JID innovations : skin science from molecules to population health · 2025
    Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. 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

13 authors at 4 institutions in 2 countries.

Yaqun Huang *Department of Dermatology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Da Liu *Department of Dermatology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Mengting ChenDepartment of Dermatology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
San XuDepartment of Dermatology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Qinqin PengDepartment of Dermatology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Yan ZhuDepartment of Dermatology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Juan LongDepartment of Dermatology, Hunan Children's Hospital, Changsha, Hunan, China.
Tangxiele LiuDepartment of Dermatology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Zhili DengDepartment of Dermatology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Hongfu XieDepartment of Dermatology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Ji LiDepartment of Dermatology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Fangfen LiuDepartment of Dermatology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Wenqin XiaoDepartment of Dermatology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
National Clinical Research · USXiangya Hospital Central South University · CNCentral South University · CNHunan Children's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rosacea is a chronic inflammatory skin disease originated from damaged skin barrier and innate/adaptive immune dysregulation. Toll-like receptors (TLRs) sense injured skin and initiate downstream inflammatory and immune responses, whose role in rosacea is not fully understood. Here, via RNA-sequencing analysis, we found that the TLR signaling pathway is the top-ranked signaling pathway enriched in rosacea skin lesions, in which TLR7 is highlighted and positively correlated with the inflammation severity of disease. In LL37-induced rosacea-like mouse models, silencing TLR7 prevented the development of rosacea-like skin inflammation. Specifically, we demonstrated that overexpressing TLR7 in keratinocytes stimulates rapamycin-sensitive mTOR complex 1 (mTORC1) pathway

Indexed as

DermatitisRosaceaToll-Like Receptor 7AnimalsInflammationMechanistic Target of Rapamycin Complex 1Membrane GlycoproteinsMiceNF-kappa BSkinMechanistic Target of Rapamycin Complex 1Membrane GlycoproteinsNF-kappa BTlr7 protein, mouseToll-Like Receptor 7MTORNFκBRosaceaSkin immunologySkin inflammationTLR7

Identifiers

PMID37780385
PMCPMC10540772
OpenAlexW4387052124

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.