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

Inactivation of the transcription factor STAT-4 prevents inflammation-driven fibrosis in animal models of systemic sclerosis.

Arthritis and rheumatism - 1 Mar 2011

Avouac Jérôme, Fürnrohr Barbara G, Tomcik Michal, Palumbo Katrin, Zerr Pawel, Horn Angelika, Dees Clara, Akhmetshina Alfiya, Beyer Christian, Distler Oliver, Schett Georg, Allanore Yannick, Distler Jörg H W

Abstract excerpt

OBJECTIVE: The transcription factor STAT-4 has recently been identified as a genetic susceptibility factor in systemic sclerosis (SSc) and other autoimmune diseases. The aim of this study was to investigate the contribution of STAT-4 in the development of a fibrotic phenotype in 2 different mouse models of experimental dermal fibrosis. METHODS: STAT-4-deficient (stat4(-/-) ) mice and their wild-type littermates...

Read the complete abstract on PubMed

Topics

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

Share to Antibiotics, Antineoplastic
Share to Bleomycin

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Dermis

Share to Fibrosis

Share to Inflammation

Share to Scleroderma, Systemic

Share to Skin Diseases

Share to STAT4 Transcription Factor

Source

Identifiers

PMID: 21360510
DOI: 10.1002/art.30171

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Inactivation of the transcription factor STAT-4 prevents inflammation-driven fibrosis in animal models of systemic sclerosis.PMID 21360510Read ↗

Multifaceted contribution of the TLR4-activated IRF5 transcription factor in systemic sclerosisSemantic proximity Read ↗

Identification of Optimal Mouse Models of Systemic Sclerosis by Interspecies Comparative GenomicsSemantic proximity Read ↗

Activation of STAT3 integrates common profibrotic pathways to promote fibroblast activation and tissue fibrosisSemantic proximity Read ↗

Targeting transcription factor Stat4 uncovers a role for interleukin-18 in the pathogenesis of severe lupus nephritis in miceSemantic proximity Read ↗

STAT4 is a genetic risk factor for systemic sclerosis having additive effects with IRF5 on disease susceptibility and related pulmonary fibrosis.Semantic proximity Read ↗

Effect of targeted disruption of STAT4 and STAT6 on the induction of experimental autoimmune encephalomyelitisSemantic proximity Read ↗

STAT4 deficiency reduces autoantibody production and glomerulonephritis in a mouse model of lupusSemantic proximity Read ↗

Fibroblast-specific Stat1 deletion enhances the myofibroblast phenotype during tissue repair.Semantic proximity Read ↗

Effect of targeted disruption of STAT4 and STAT6 on the induction of experimental autoimmune encephalomyelitisSemantic proximity Read ↗

BAFF antagonist attenuates the development of skin fibrosis in tight-skin mice.Semantic proximity Read ↗

IL-4 regulates skin homeostasis and the predisposition toward allergic skin inflammation.Semantic proximity Read ↗

Understanding the Role of Epithelial Cells in the Pathogenesis of Systemic SclerosisSemantic proximity Read ↗

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