Evidence map›Paper›PMID 34207510›Full record

ReviewInternational journal of molecular sciences2021

Role of JAK/STAT in Interstitial Lung Diseases; Molecular and Cellular Mechanisms.

Paula Montero, Javier Milara, Inés Roger, Julio Cortijo

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 144 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
144citing papers in PubMed, 3 pooled it
25.1field-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

144 citing papers in PubMed, 3 syntheses or guidelines pooled it, 235 citations in OpenAlex.

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  12. Erythropoietin and Ferulic Acid Loaded on FeApplied biochemistry and biotechnology · 2026
    Article
  13. [Clinical characteristics and outcomes of children with rheu-matoid factor-positive polyarticular juvenile idiopathic arthritis].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2026
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84 more citing papers are in PubMed but not listed here.

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

4 authors at 1 institution in 1 country.

Paula MonteroDepartment of Pharmacology, Faculty of Medicine, University of Valencia, 46010 Valencia, Spain.
Javier MilaraDepartment of Pharmacology, Faculty of Medicine, University of Valencia, 46010 Valencia, Spain.
Inés RogerDepartment of Pharmacology, Faculty of Medicine, University of Valencia, 46010 Valencia, Spain.
Julio CortijoDepartment of Pharmacology, Faculty of Medicine, University of Valencia, 46010 Valencia, Spain.
Universitat de València · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Interstitial lung diseases (ILDs) comprise different fibrotic lung disorders characterized by cellular proliferation, interstitial inflammation, and fibrosis. The JAK/STAT molecular pathway is activated under the interaction of a broad number of profibrotic/pro-inflammatory cytokines, such as IL-6, IL-11, and IL-13, among others, which are increased in different ILDs. Similarly, several growth factors over-expressed in ILDs, such as platelet-derived growth factor (PDGF), transforming growth factor β1 (TGF-β1), and fibroblast growth factor (FGF) activate JAK/STAT by canonical or non-canonical pathways, which indicates a predominant role of JAK/STAT in ILDs. Between the different JAK/STAT isoforms, it appears that JAK2/STAT3 are predominant, initiating cellular changes observed in ILDs. This review analyzes the expression and distribution of different JAK/STAT isoforms in ILDs lung tissue and different cell types related to ILDs, such as lung fibroblasts and alveolar epithelial type II cells and analyzes JAK/STAT activation. The effect of JAK/STAT phosphorylation on cellular fibrotic processes, such as proliferation, senescence, autophagy, endoplasmic reticulum stress, or epithelial/fibroblast to mesenchymal transition will be described. The small molecules directed to inhibit JAK/STAT activation were assayed in vitro and in in vivo models of pulmonary fibrosis, and different JAK inhibitors are currently approved for myeloproliferative disorders. Recent evidence indicates that JAK inhibitors or monoclonal antibodies directed to block IL-6 are used as compassionate use to attenuate the excessive inflammation and lung fibrosis related to SARS-CoV-2 virus. These altogether indicate that JAK/STAT pathway is an attractive target to be proven in future clinical trials of lung fibrotic disorders.

Indexed as

Cellular SenescenceEndoplasmic Reticulum StressHumansInterleukinsJanus KinasesLung Diseases, InterstitialProtein IsoformsProtein Kinase InhibitorsSignal TransductionSTAT Transcription FactorsInterleukinsJanus KinasesProtein IsoformsProtein Kinase InhibitorsSTAT Transcription Factorsidiopathic pulmonary fibrosis (IPF)interstitial lung disease (ILD)Janus kinases (JAK)signal transducer and activator of transcription (STAT)

Identifiers

PMID34207510
PMCPMC8226626
OpenAlexW3170001459

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.