Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

EGR1/NOX4 pathway regulates oxidative stress and further facilitates fibrosis progression in keloids responses to TGF-β1

1 Dec 2022

Abstract excerpt

BACKGROUND: As classic benign fibroproliferative tumors, keloids remain a major therapeutic challenge due to their complex pathological mechanisms. OBJECTIVE: To determine the functional role of transforming growth factor β1 (TGF-β1)/early growth response factor-1 (EGR1)/NADPH oxidases 4 (NOX4) axis in the pathogenesis of keloid fibrosis. METHODS: Differentially expressed genes in keloid tissues and normal skins...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Dermatologic Treatments and Research
Share to Fibroblast Growth Factor Research
Share to Wound Healing and Treatments

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 36608994
DOI: 10.1016/j.jdermsci.2022.12.009

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

EGR1/NOX4 pathway regulates oxidative stress and further facilitates fibrosis progression in keloids responses to TGF-β1PMID 36608994Read ↗

Identification of Key Gene and Pathways Associated with Oxidative Stress in KeloidsSemantic proximity Read ↗

Transforming growth factor beta (TGFβ) and keloid diseaseSemantic proximity Read ↗

Hypoxia drives the transition of human dermal fibroblasts to a myofibroblast-like phenotype via the TGF-β1/Smad3 pathway.Semantic proximity Read ↗

Keloids – clinical diagnosis, pathogenesis, and treatment optionsSemantic proximity Read ↗

NADPH oxidase 4 is dispensable for skin myofibroblast differentiation and wound healingSemantic proximity Read ↗

Molecular dissection of abnormal wound healing processes resulting in keloid diseaseSemantic proximity Read ↗

EDN1 and NTF3 in keloid pathogenesis: computational and experimental evidence as novel diagnostic biomarkers for fibrosis and inflammationSemantic proximity Read ↗

Identification of novel biomarkers of ferroptosis involved in keloid based on bioinformatics analysisSemantic proximity Read ↗

Multitranscriptome analyses of keloid fibroblasts reveal the role of the HIF-1α/HOXC6/ERK axis in keloid developmentSemantic proximity Read ↗

Screening of keloid immune microenvironment-related genes and their effects on keloid proliferation and migrationSemantic proximity Read ↗

Treatment of keloids through Runx2 siRNA‑induced inhibition of the PI3K/AKT signaling pathwaySemantic proximity Read ↗

BMP1 Promotes Keloid by Inducing Fibroblast Inflammation and FibrogenesisSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.