Evidence map›Paper›PMID 36768203›Full record

ReviewInternational journal of molecular sciences2023

Fli1 and Tissue Fibrosis in Various Diseases.

Elena V Mikhailova, Irina V Romanova, Alexei Y Bagrov, Natalia I Agalakova

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

9 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. From moderate to strenuous training: unravelling mechanistic contributors and biomarkers for atrial fibrillation in exercise.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2025
    Article
  6. Review
  7. Article
  8. EP300 as a Molecular Integrator of Fibrotic Transcriptional Programs.International journal of molecular sciences · 2023
    Review
  9. Article
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.

Elena V MikhailovaSechenov Institute of Evolutionary Physiology and Biochemistry, Russian Academy of Sciences, 44 Thorez Avenue, 194223 Saint-Petersburg, Russia.
Irina V RomanovaSechenov Institute of Evolutionary Physiology and Biochemistry, Russian Academy of Sciences, 44 Thorez Avenue, 194223 Saint-Petersburg, Russia.ORCID 0000-0002-0348-0631
Alexei Y BagrovPadakonn Pharma, 20309 Narva, Estonia.ORCID 0000-0002-2903-8673
Natalia I AgalakovaSechenov Institute of Evolutionary Physiology and Biochemistry, Russian Academy of Sciences, 44 Thorez Avenue, 194223 Saint-Petersburg, Russia.
Institute of Evolutionary Physiology and Biochemistry · RU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Being initially described as a factor of virally-induced leukemias, Fli1 (Friend leukemia integration 1) has attracted considerable interest lately due to its role in both healthy physiology and a variety of pathological conditions. Over the past few years, Fli1 has been found to be one of the crucial regulators of normal hematopoiesis, vasculogenesis, and immune response. However, abnormal expression of Fli1 due to genetic predisposition, epigenetic reprogramming (modifications), or environmental factors is associated with a few diseases of different etiology. Fli1 hyperexpression leads to malignant transformation of cells and progression of cancers such as Ewing's sarcoma. Deficiency in Fli1 is implicated in the development of systemic sclerosis and hypertensive disorders, which are often accompanied by pronounced fibrosis in different organs. This review summarizes the initial findings and the most recent advances in defining the role of Fli1 in diseases of different origin with emphasis on its pro-fibrotic potential.

Indexed as

Sarcoma, EwingScleroderma, SystemicFibrosisHumansOncogene Proteins, FusionProto-Oncogene Protein c-fli-1RNA-Binding Protein EWSFLI1 protein, humanOncogene Proteins, FusionProto-Oncogene Protein c-fli-1RNA-Binding Protein EWSangiogenesisEwing’s sarcomafibrosisFli1preeclampsiasystemic sclerosisuremic cardiomyopathy

Identifiers

PMID36768203
PMCPMC9915382
OpenAlexW4317518430

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.