Evidence map›Paper›PMID 31614787›Full record

ReviewInternational journal of molecular sciences2019

Gas6/TAM System: A Key Modulator of the Interplay between Inflammation and Fibrosis.

Mattia Bellan, Micol Giulia Cittone, Stelvio Tonello, Cristina Rigamonti, Luigi Mario Castello, Francesco Gavelli, Mario Pirisi, Pier Paolo Sainaghi

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

58 citing papers in PubMed, 86 citations in OpenAlex.

  1. Article
  2. Article
  3. 3D-bioprinted adipose-derived stem cell-secreted GAS6Journal of nanobiotechnology · 2026
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. The functional role of the extracellular matrix in inflammatory bowel disease associated gut fibrosis.Matrix biology : journal of the International Society for Matrix Biology · 2025
    Review
  13. Recent advances in TAM mechanisms in lung diseases.Journal of translational medicine · 2025
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

8 authors at 1 institution in 1 country.

Mattia BellanDepartment of Translational Medicine, Università del Piemonte Orientale UPO, 28100 Novara, Italy. mattia.bellan@med.uniupo.it.ORCID 0000-0003-1488-8736
Micol Giulia CittoneDepartment of Translational Medicine, Università del Piemonte Orientale UPO, 28100 Novara, Italy. micolcittone@gmail.com.
Stelvio TonelloDepartment of Translational Medicine, Università del Piemonte Orientale UPO, 28100 Novara, Italy. stelvio.tonello@med.uniupo.it.
Cristina RigamontiDepartment of Translational Medicine, Università del Piemonte Orientale UPO, 28100 Novara, Italy. crigamo@tin.it.
Luigi Mario CastelloDepartment of Translational Medicine, Università del Piemonte Orientale UPO, 28100 Novara, Italy. luigi.castello@med.uniupo.it.ORCID 0000-0001-8248-1976
Francesco GavelliDepartment of Translational Medicine, Università del Piemonte Orientale UPO, 28100 Novara, Italy. gavelli.francesco@gmail.com.ORCID 0000-0002-0581-245X
Mario PirisiDepartment of Translational Medicine, Università del Piemonte Orientale UPO, 28100 Novara, Italy. mario.pirisi@med.uniupo.it.
Pier Paolo SainaghiDepartment of Translational Medicine, Università del Piemonte Orientale UPO, 28100 Novara, Italy. pierpaolo.sainaghi@med.uniupo.it.ORCID 0000-0001-8322-9158
Università degli Studi del Piemonte Orientale “Amedeo Avogadro” · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fibrosis is the result of an overly abundant deposition of extracellular matrix (ECM) due to the fact of repetitive tissue injuries and/or dysregulation of the repair process. Fibrogenesis is a pathogenetic phenomenon which is involved in different chronic human diseases, accounting for a high burden of morbidity and mortality. Despite being triggered by different causative factors, fibrogenesis follows common pathways, the knowledge of which is, however, still unsatisfactory. This represents a significant limit for the development of effective antifibrotic drugs. In the present paper, we aimed to review the current evidence regarding the potential role played in fibrogenesis by growth arrest-specific 6 (Gas6) and its receptors Tyro3 protein tyrosine kinase (Tyro3), Axl receptor tyrosine kinase (Axl), and Mer tyrosine kinase protooncogene (MerTK) (TAM). Moreover, we aimed to review data about the pathogenetic role of this system in the development of different human diseases characterized by fibrosis. Finally, we aimed to explore the potential implications of these findings in diagnosis and treatment.

Indexed as

AnimalsCardiovascular Systemc-Mer Tyrosine KinaseFibrosisGrowth Arrest-Specific Protein 6HumansInflammationIntercellular Signaling Peptides and ProteinsLiverLiver CirrhosisLungc-Mer Tyrosine KinaseGrowth Arrest-Specific Protein 6Intercellular Signaling Peptides and ProteinsAxlcirrhosisfibrosisGas6inflammationIPFMerTKTAM

Identifiers

PMID31614787
PMCPMC6834320
OpenAlexW2979361795

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.