Evidence map›Paper›PMID 42352350›Full record

ReviewBiomolecules2026

The Matrix Reloaded: The Hepatic Matrisome as a Therapeutic Opportunity to Fight Liver Fibrosis.

Cristina Benavides, Pepa Kecheva, Fernando Solano, Olga Martínez-Arroyo, Juan V Esplugues, Ana Blas-García, Nadezda Apostolova

Abstract readReview
In one paragraph

Review in Biomolecules, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

7 authors.

Cristina BenavidesDepartamento de Farmacología, Facultad de Medicina, Universitat de València, 46010 Valencia, Spain.ORCID 0000-0002-5079-2267
Pepa KechevaDepartamento de Fisiología, Facultad de Medicina, Universitat de València, 46010 Valencia, Spain.
Fernando SolanoDepartamento de Farmacología, Facultad de Medicina, Universitat de València, 46010 Valencia, Spain.ORCID 0009-0001-0408-4622
Olga Martínez-ArroyoDepartamento de Farmacología, Facultad de Medicina, Universitat de València, 46010 Valencia, Spain.ORCID 0000-0001-9602-8419
Juan V EspluguesDepartamento de Farmacología, Facultad de Medicina, Universitat de València, 46010 Valencia, Spain.ORCID 0000-0001-8205-021X
Ana Blas-GarcíaFISABIO-Hospital Universitario Dr. Peset, 46017 Valencia, Spain.ORCID 0000-0001-7870-1470
Nadezda ApostolovaDepartamento de Farmacología, Facultad de Medicina, Universitat de València, 46010 Valencia, Spain.ORCID 0000-0002-4487-2471

Funding

Generalitat Valenciana CIGRIS/2022/133Generalitat Valenciana CIGRIS/2023/10Generalitat Valenciana CIPROM/2021/044Instituto de Salud Carlos III CIBER CB06/04/0071Ministerio de Ciencia, Innovación y Universidades PID2024-159385OB-I00
6 · The paper itself

Abstract

Liver fibrosis is the excessive accumulation of extracellular matrix (ECM) that occurs in most types of chronic liver diseases (CLDs) as a response to sustained liver injury. While the ECM comprises different proteins, collagen being the most abundant, the term matrisome refers to a plethora of ECM-related molecules, including collagen-associated proteins, growth factors, cytokines, enzymes and their endogenous inhibitors. The hepatic matrisome undergoes significant qualitative and quantitative changes during liver fibrosis. Despite intense research over recent years, our understanding of the matrisome in the liver-both in health and disease-and particularly of its function beyond its conventional structural role, remains poor. This review highlights how comprehending hepatic matrisome responses to liver injury can yield novel insights into disease progression and regression and could be exploited as a potential antifibrotic strategy. The antifibrotic potency of drugs that interfere with the matrisome at different levels has been demonstrated in preclinical studies, but translation to clinical trials remains still limited. So far, simtuzumab (LOXL2 inhibitor antibody), imatinib (small-molecule inhibitor against discoidin domain receptors-DDRs), bexotegrast (integrin inhibitor), GR-MD-02 (galectin 3 inhibitor), and BMS-986263 (siRNA-targeting HSP47) have been or are being evaluated in clinical trials related to CLD, and some of them have shown promising results.

Indexed as

Extracellular MatrixExtracellular Matrix ProteinsLiverLiver CirrhosisAnimalsCollagenHumansCollagenExtracellular Matrix Proteinscollagenextracellular matrixhepatic stellate cellsliver fibrosistherapeutic targets

Identifiers

PMID42352350
PMCPMC13296903

What OpenQuestion holds

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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 OpenQuestion graph.