Evidence map›Paper›PMID 16380822›Full record

ReviewJournal of clinical immunology2005

Molecular aspects of regulation of collagen gene expression in fibrosis.

Rashpal K Bhogal, Cristina M Stoica, Tracy L McGaha, Constantin A Bona

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of clinical immunology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
2.5field-weighted citation impact, top 12% 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

43 citing papers in PubMed, 89 citations in OpenAlex.

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  17. siRNA- and miRNA-based therapeutics for liver fibrosis.Translational research : the journal of laboratory and clinical medicine · 2019
    Review
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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

4 authors at 2 institutions in 1 country.

Rashpal K BhogalDepartment of Microbiology, Mount Sinai School of Medicine, One Gustave L. Levy Place, New York, NY 10029, USA.
Cristina M Stoica
Tracy L McGaha
Constantin A Bona
Icahn School of Medicine at Mount Sinai · USMount Sinai Hospital · US

Funding

Molecular studies on the role of IL4 &IL13 in fibrosisR01AI055737 · NIAID · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI BONA, CONSTANTIN A · 2004 to 2008
$1.5M
NIAID NIH HHS R01 AI 55737
6 · The paper itself

Abstract

Fibrosis, the hyper-accumulation of scar tissue, is characterized by the overproduction and deposition of type I and III collagen by fibroblasts and is the one of the main pathologic outcomes of the autoimmune disorder scleroderma. While the causes of fibrosis in scleroderma are unknown, cytokines such as TGF-beta, IL-4 and IL-13, play a crucial role in the stimulation of collagen production have been implicated in the disease process. In fibroblasts stimulation of collagen production by these cytokines is dependent on the Smad and STAT6 signaling pathways induced by TGF-beta and IL-4, IL-13 respectively. Furthermore, mounting evidence suggest cytokine crosstalk is relevant in the sclerotic process. Our laboratory demonstrated an increase in TGF-beta1 gene transcription from fibroblasts stimulated with IL-4. In addition, TSK/+ mice lacking the IL-4alpha receptor show impaired transcription of the TGF-beta1 gene and did not display fibrosis. Likewise, it appears that STAT6 plays a role in fibroblast TGF-beta1 transcription after IL-4 or IL-13 stimulation. These findings suggest that an epistatic interaction between IL-4 and TGF-beta may exist which is crucial for pathologic sclerotic activity.

Indexed as

AnimalsCollagenFibroblastsFibrosisGene Expression RegulationHumansInflammationCollagen

Identifiers

PMID16380822
OpenAlexW2003422642

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.