Evidence map›Paper›PMID 41065540›Full record

ArticleMolecular oncology2026

Modeling hepatic fibrosis in TP53 knockout iPSC-derived human liver organoids.

Mustafa Karabicici, Soheil Akbari, Ceyda Caliskan, Canan Celiker, Ozden Oz, Leman Binokay, Gökhan Karakulah, Serif Senturk, Esra Erdal

Abstract read
In one paragraph

Article in Molecular oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. A practical toolbox for modelling fibrosis in vitro.Nature biomedical engineering · 2026
    Review
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

9 authors.

Mustafa KarabiciciIzmir Biomedicine and Genome Center (IBG), Dokuz Eylul University Health Campus, Izmir, Turkey.ORCID https://orcid.org/0000-0002-0359-7645
Soheil AkbariIzmir Biomedicine and Genome Center (IBG), Dokuz Eylul University Health Campus, Izmir, Turkey.
Ceyda CaliskanIzmir Biomedicine and Genome Center (IBG), Dokuz Eylul University Health Campus, Izmir, Turkey.
Canan CelikerIzmir International Biomedicine and Genome Institute (IBG-Izmir), Dokuz Eylul University, Izmir, Turkey.
Ozden OzIzmir Biomedicine and Genome Center (IBG), Dokuz Eylul University Health Campus, Izmir, Turkey.
Leman BinokayIzmir Biomedicine and Genome Center (IBG), Dokuz Eylul University Health Campus, Izmir, Turkey.
Gökhan KarakulahIzmir Biomedicine and Genome Center (IBG), Dokuz Eylul University Health Campus, Izmir, Turkey.
Serif SenturkIzmir Biomedicine and Genome Center (IBG), Dokuz Eylul University Health Campus, Izmir, Turkey.ORCID https://orcid.org/0000-0003-3963-2294
Esra ErdalIzmir Biomedicine and Genome Center (IBG), Dokuz Eylul University Health Campus, Izmir, Turkey.ORCID https://orcid.org/0000-0001-7264-0574

Funding

Türkiye Bilimsel ve Teknolojik Araştırma Kurumu 1001: 117Z858Türkiye Bilimsel ve Teknolojik Araştırma Kurumu 1002: 221Z357
6 · The paper itself

Abstract

Hepatic fibrogenesis is characterized by the excessive accumulation of extracellular matrix proteins, ultimately predisposing to hepatocarcinogenesis. The lack of reliable models that faithfully recapitulate early stage fibrogenesis is one of the main limitations in identifying translationally relevant therapeutics. Here, we establish a model using CRISPR/Cas9-mediated TP53 knockout iPSC (endoderm)-derived human hepatic organoids (eHEPOs) to mimic human liver fibrosis. Transcriptomic profiling of TP53KO-eHEPOs revealed enrichment of pathways associated with inflammation, ECM remodeling, and fibrosis, with notable alterations in pivotal fibrotic regulators. We also find increased expression of myofibroblasts and fibrosis markers (PDGFRB, COL1A1, COL3A1, COL11A1) and early liver cancer markers (GPC3 and MUC1). Histological analysis confirmed advanced fibrotic hallmarks and exposure to an exogenous profibrotic environment (pf-ME) further enhanced these fibrotic phenotypes. This model provides a valuable platform for exploring the role of key driver genes, such as TP53, in the initiation and progression of fibrosis, enabling the study of hepatic progenitor cell transformation across diverse microenvironmental contexts. As such, it holds the potential for advancing early stage drug discovery and the identification of novel therapeutic targets for the treatment of liver fibrosis.

Indexed as

Gene Knockout TechniquesInduced Pluripotent Stem CellsLiverLiver CirrhosisModels, BiologicalOrganoidsTumor Suppressor Protein p53Gene Expression ProfilingHumansTP53 protein, humanTumor Suppressor Protein p53CRISPR/Cas9extracellular matrix remodelingiPSC‐derived organoidsliver fibrosisTP53 knockout

Identifiers

PMID41065540
PMCPMC13042547

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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.