Evidence map›Paper›PMID 38298195›Full record

ReviewFrontiers in immunology2024

From MASH to HCC: the role of Gas6/TAM receptors.

Daria Apostolo, Luciana L Ferreira, Federica Vincenzi, Nicole Vercellino, Rosalba Minisini, Federico Latini, Barbara Ferrari, Michela E Burlone, Mario Pirisi, Mattia Bellan

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

13 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Fibrinogen superfamily proteins: Key regulators in hepatic disorders.World journal of experimental medicine · 2025
    Review
  5. Article
  6. Targeting Metabolism: Innovative Therapies for MASLD Unveiled.International journal of molecular sciences · 2025
    Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Review
  12. Review
  13. MRTO4 Enhances Glycolysis to Facilitate HCC Progression by Inhibiting ALDOB.Medical science monitor : international medical journal of experimental and clinical research · 2024
    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

10 authors at 2 institutions in 1 country.

Daria ApostoloDepartment of Translational Medicine, Università del Piemonte Orientale, Novara, Italy.
Luciana L FerreiraDepartment of Translational Medicine, Università del Piemonte Orientale, Novara, Italy.
Federica VincenziDepartment of Translational Medicine, Università del Piemonte Orientale, Novara, Italy.
Nicole VercellinoDepartment of Translational Medicine, Università del Piemonte Orientale, Novara, Italy.
Rosalba MinisiniDepartment of Translational Medicine, Università del Piemonte Orientale, Novara, Italy.
Federico LatiniDepartment of Translational Medicine, Università del Piemonte Orientale, Novara, Italy.
Barbara FerrariDepartment of Translational Medicine, Università del Piemonte Orientale, Novara, Italy.
Michela E BurloneDepartment of Internal Medicine, Azienda Ospedaliero-Universitaria Maggiore Della Carità, Novara, Italy.
Mario PirisiDepartment of Translational Medicine, Università del Piemonte Orientale, Novara, Italy.
Mattia BellanDepartment of Translational Medicine, Università del Piemonte Orientale, Novara, Italy.
Università degli Studi del Piemonte Orientale “Amedeo Avogadro” · ITAzienda Ospedaliero Universitaria Maggiore della Carita · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metabolic dysfunction-associated steatohepatitis (MASH) is the replacement term for what used to be called nonalcoholic steatohepatitis (NASH). It is characterized by inflammation and injury of the liver in the presence of cardiometabolic risk factors and may eventually result in the development of hepatocellular carcinoma (HCC), the most common form of primary liver cancer. Several pathogenic mechanisms are involved in the transition from MASH to HCC, encompassing metabolic injury, inflammation, immune dysregulation and fibrosis. In this context, Gas6 (Growth Arrest-Specific 6) and TAM (Tyro3, Axl, and MerTK) receptors may play important roles. The Gas6/TAM family is involved in the modulation of inflammation, lipid metabolism, fibrosis, tumor progression and metastasis, processes which play an important role in the pathophysiology of acute and chronic liver diseases. In this review, we discuss MASH-associated HCC and the potential involvement of the Gas6/TAM system in disease development and progression. In addition, since therapeutic strategies for MASH and HCC are limited, we also speculate regarding possible future treatments involving the targeting of Gas6 or TAM receptors.

Indexed as

Carcinoma, HepatocellularFatty LiverLiver NeoplasmsFibrosisHumansInflammationProto-Oncogene ProteinsProto-Oncogene ProteinsGas6HCCliverMASHMASLDNAFLDNASHTAM receptors

Identifiers

PMID38298195
PMCPMC10827955
OpenAlexW4390953345

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.