Evidence map›Paper›PMID 40980160›Full record

ArticleJHEP reports : innovation in hepatology2025

GTX-11 improves portal hypertension, liver fibrosis, and sinusoidal cells phenotype in experimental MASH.

María Andrés-Rozas, Zoe Boyer-Diaz, Eugènia Ruiz-Cánovas, Peio Aristu-Zabalza, Sergi Guixé-Muntet, Cristina Fernández-Asensio, Juan José Lozano, Noemí García-Delgado, Carla Fuster, Jaume Mercade and 2 more

Abstract read
In one paragraph

Article in JHEP reports : innovation in hepatology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Review
  2. Article
  3. 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

12 authors.

María Andrés-RozasBarcelona Liver Bioservices, Barcelona, Spain.
Zoe Boyer-DiazBarcelona Liver Bioservices, Barcelona, Spain.
Eugènia Ruiz-CánovasGAT Therapeutics, Barcelona, Spain.
Peio Aristu-ZabalzaBarcelona Liver Bioservices, Barcelona, Spain.
Sergi Guixé-MuntetLiver Vascular Biology Research Group, IDIBAPS - Hospital Clínic Barcelona, Barcelona, Spain.
Cristina Fernández-AsensioGAT Therapeutics, Barcelona, Spain.
Juan José LozanoCentro de Investigación Biomédica en Red en Enfermedades Hepáticas y Digestivas (CIBEREHD), Instituto de Salud Carlos III (ISCIII), Madrid, Spain.
Noemí García-DelgadoGAT Therapeutics, Barcelona, Spain.
Carla FusterDepartment of Pathology, Hospital Clínic de Barcelona, Spain.
Jaume MercadeGAT Therapeutics, Barcelona, Spain.
Jaime BoschLiver Vascular Biology Research Group, IDIBAPS - Hospital Clínic Barcelona, Barcelona, Spain.
Jordi Gracia-SanchoBarcelona Liver Bioservices, Barcelona, Spain.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background & Aims: Steatotic liver disease can lead to the development of metabolic dysfunction-associated steatohepatitis (MASH), the prevalence of which is rapidly increasing, intensifying the need to find an effective treatment. GTX-11 is a first-in-class drug with anti-inflammatory and antifibrotic properties mediated by the modulation of the transforming growth factor beta pathway. The present study evaluated the effects of GTX-11 on hepatic hemodynamics and liver fibrosis, as well as its underlying mechanisms, in a preclinical model of MASH, and in human precision-cut liver slices (hPCLS). Methods: Male Wistar MASH rats received GTX-11 (1 and 10 mg/kg/day) or vehicle, for 14 days (n = 15/group). Results: MASH rats receiving GTX-11 showed a significant dose-dependent reduction in portal pressure compared with the vehicle (-8.4% Conclusions: This study demonstrates for the first time the beneficial effects of GTX-11 on portal hypertension and liver fibrosis in MASH by means of HSCs deactivation and endothelial phenotype restoration. Validation in human liver tissues encourages its clinical evaluation as a possible new treatment for this disease. Impact and implications: Metabolic dysfunction-associated steatohepatitis (MASH) affects >3-6% of the world's population, and this number continues to increase. Despite its high prevalence, there is currently no specific, generally effective, and safe treatment for the disease. This study demonstrates, for the first time, the therapeutic potential of GTX-11 in treating fibrosis and portal hypertension associated with MASH by deactivating hepatic stellate cells and enhancing endothelial phenotype. These findings highlight GTX-11 as a promising candidate for future therapeutic strategies aimed at reversing liver fibrosis and improving patient outcomes in MASH.

Indexed as

HSCLiver cirrhosisLSECMASLDPortal hypertension

Identifiers

PMID40980160
PMCPMC12447985

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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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 Socratic graph.