Evidence map›Paper›PMID 35382402›Full record

ArticleJournal of scleroderma and related disorders2020

The JAK/STAT pathway is activated in systemic sclerosis and is effectively targeted by tofacitinib.

Wenxia Wang, Swati Bhattacharyya, Roberta Goncalves Marangoni, Mary Carns, Kathleen Dennis-Aren, Anjana Yeldandi, Jun Wei, John Varga

Open access · bronzeAbstract read
In one paragraph

Article in Journal of scleroderma and related disorders, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed, 2 pooled it
6.5field-weighted citation impact, top 3% 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

50 citing papers in PubMed, 2 syntheses or guidelines pooled it, 90 citations in OpenAlex.

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  18. Fibroblast Heterogeneity in Inflammatory Bowel Disease.International journal of molecular sciences · 2024
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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 1 institution in 1 country.

Wenxia WangNorthwestern Scleroderma Program, Division of Rheumatology, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
Swati BhattacharyyaNorthwestern Scleroderma Program, Division of Rheumatology, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.ORCID https://orcid.org/0000-0002-4005-5896
Roberta Goncalves MarangoniNorthwestern Scleroderma Program, Division of Rheumatology, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
Mary CarnsNorthwestern Scleroderma Program, Division of Rheumatology, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
Kathleen Dennis-ArenNorthwestern Scleroderma Program, Division of Rheumatology, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
Anjana YeldandiDepartment of Surgical Pathology, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
Jun WeiNorthwestern Scleroderma Program, Division of Rheumatology, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
John VargaNorthwestern Scleroderma Program, Division of Rheumatology, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
Northwestern University · US

Funding

REGULATION OF COLLAGEN GENE EXPRESSION BY TGF-BETAR01AR042309 · NIAMS · UNIVERSITY OF ILLINOIS AT CHICAGO · PI VARGA, JOHN · 1994 to 2014
$4.4M
Aberrant TLR responses driving organ fibrosis in systemic sclerosisR56AR042309 · NIAMS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI VARGA, JOHN · 2018 to 2018
$477k
NIAMS NIH HHS R01 AR042309NIAMS NIH HHS R56 AR042309
6 · The paper itself

Abstract

Rationale: Fibrosis leads to failure of the skin, lungs, and other organs in systemic sclerosis; accounts for substantial morbidity and mortality; and lacks effective therapy. Myofibroblast activation underlies organ fibrosis, but the key extracellular cues driving persistence of the process remain incompletely characterized. Objectives: The objectives were to evaluate activation of the IL6/JAK/STAT axis associated with fibrosis in skin and lung biopsies from systemic sclerosis patients and effects of the Food and Drug Administration-approved JAK/STAT inhibitor, tofacitinib, on skin and lung fibrosis in animal models. Methods: Bioinformatic analysis showed that IL6/JAK/STAT3 and tofacitinib gene signatures were aberrant in biopsies from systemic sclerosis patients in four independent cohorts. The results were confirmed by JAK and STAT3 phosphorylation in both skin and lung biopsies from patients with systemic sclerosis. Furthermore, treatment of mice with the selective JAK inhibitor tofacitinib not only prevented bleomycin-induced skin and lung fibrosis but also reduced skin fibrosis in TSK1/+ mice. Conclusion: These findings implicate the JAK/STAT pathway in systemic sclerosis skin and lung fibrosis and identify tofacitinib as a potential antifibrotic agent for the treatment of systemic sclerosis and other fibrotic diseases.

Indexed as

fibrosisinterleukin 6JAKSTAT3systemic sclerosisTofacitinib

Identifiers

PMID35382402
PMCPMC8922593
OpenAlexW2965426852

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.