Evidence map›Paper›PMID 31645185›Full record

ArticleCell cycle (Georgetown, Tex.)2019

HIF-1α promotes the keloid development through the activation of TGF-β/Smad and TLR4/MyD88/NF-κB pathways.

Rui Lei, Jian Li, Feng Liu, Weihan Li, Shizhen Zhang, Yang Wang, Xi Chu, Jinghong Xu

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
10.5field-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

58 citing papers in PubMed, 100 citations in OpenAlex.

  1. Trial
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  12. Article
  13. LangerinClinical, cosmetic and investigational dermatology · 2025
    Review
  14. Article
  15. Article
  16. Update on the Pathogenesis of Keloid Formation.JID innovations : skin science from molecules to population health · 2024
    Review
  17. Article
  18. Review
  19. Promising predictive molecular biomarkers for cervical cancer (Review).International journal of molecular medicine · 2024
    Review
  20. miRSNP rs188493331: A key player in genetic control of microRNA-induced pathway activation in hypertrophic scars and keloids.Skin research and technology : official journal of International Society for Bioengineering and the Skin (ISBS) [and] International Society for Digital Imaging of Skin (ISDIS) [and] International Society for Skin Imaging (ISSI) · 2024
    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

8 authors at 3 institutions in 1 country.

Rui LeiDepartment of Plastic Surgery, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
Jian LiDepartment of Plastic Surgery, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
Feng LiuDepartment of Plastic Surgery, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
Weihan LiDepartment of Acupuncture and Moxibustion, The Third Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, China.ORCID https://orcid.org/0000-0001-8891-4277
Shizhen ZhangInstitute of Translational Medicine, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
Yang WangDepartment of Plastic Surgery, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
Xi ChuDepartment of Plastic Surgery, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
Jinghong XuDepartment of Plastic Surgery, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
First Affiliated Hospital Zhejiang University · CNThe Third Affiliated Hospital of Zhejiang Chinese Medical University · CNZhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A keloid is defined as an overgrowth of the dense fibrous tissues that form around a wound. Since they destroy the vascular network, keloid tissues often exhibit anoxic conditions. Hypoxia-inducible factor-1α (HIF-1α) is a core factor that mediates hypoxia stress responses and regulates the hypoxic cellular and biological behaviors. In this study, we found that the expression level of HIF-1α in keloid tissue was significantly higher than that in the normal skin tissue. Hypoxia-induced HIF-1α expression significantly inhibited cellular apoptosis and promoted cellular proliferation in keloid fibroblasts but not in normal fibroblasts. Specifically, HIF-1α activated the TGF-β/Smad and TLR4/MyD88/NF-κB pathways, and the interaction of these two pathways may promote the development of keloids. Moreover,

Indexed as

AnimalsApoptosisCell HypoxiaCell ProliferationFibroblastsGene Expression RegulationHeterograftsHumansHypoxia-Inducible Factor 1, alpha SubunitKeloidMiceMyeloid Differentiation Factor 88Primary Cell CultureSignal TransductionSmad ProteinsToll-Like Receptor 4HIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitMyeloid Differentiation Factor 88RELA protein, humanSmad ProteinsTLR4 protein, humanToll-Like Receptor 4Transcription Factor RelATransforming Growth Factor betafibroblastsHIF-1αkeloidNF-κBTGF-β/SmadTLR4

Identifiers

PMID31645185
PMCPMC6927730
OpenAlexW2982040460

What OpenQuestion holds

Textmetadata
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.