Evidence map›Paper›PMID 41501149›Full record

ArticleScientific reports2026

Modeling fatty liver disease and progression with stem cell derived hepatocytes.

Yao Wang, David Berlin, Yong Li, Lok Man Ko, Zhenzhu Qi, Jiayi Feng, Christopher T Clark, Diandian Cheng, Melisa Andrade, Eric Potma and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 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

11 authors.

Yao WangDepartment of Chemical and Biomolecular Engineering, University of California, Irvine, Irvine, CA, 92697, USA.
David BerlinDepartment of Chemical and Biomolecular Engineering, University of California, Irvine, Irvine, CA, 92697, USA.
Yong LiDepartment of Chemistry, University of California, Irvine, Irvine, CA, 92697, USA.
Lok Man KoDepartment of Chemical and Biomolecular Engineering, University of California, Irvine, Irvine, CA, 92697, USA.
Zhenzhu QiDepartment of Chemical and Biomolecular Engineering, University of California, Irvine, Irvine, CA, 92697, USA.
Jiayi FengDepartment of Biomedical Engineering, University of California, Irvine, Irvine, CA, 92697, USA.
Christopher T ClarkDepartment of Chemical and Biomolecular Engineering, University of California, Irvine, Irvine, CA, 92697, USA.
Diandian ChengDepartment of Chemical and Biomolecular Engineering, University of California, Irvine, Irvine, CA, 92697, USA.
Melisa AndradeDepartment of Chemical and Biomolecular Engineering, University of California, Irvine, Irvine, CA, 92697, USA.
Eric PotmaDepartment of Chemistry, University of California, Irvine, Irvine, CA, 92697, USA.
Quinton SmithDepartment of Chemical and Biomolecular Engineering, University of California, Irvine, Irvine, CA, 92697, USA. quintons@uci.edu.

Funding

Physicochemical control of multilineage emergenceR35GM151099 · NIGMS · UNIVERSITY OF CALIFORNIA-IRVINE · PI Quinton Smith · 2023 to 2026
$1.5M
California Institute for Regenerative Medicine EDUC4-12822Howard Hughes Medical Institute GT15187NIGMS NIH HHS R35 GM151099NIH HHS R35GM151099
6 · The paper itself

Abstract

Metabolic dysfunction-associated steatotic liver disease (MASLD) is one of the most pervasive liver disorders. It can progress to metabolic dysfunction-associated steatohepatitis (MASH), hallmarked by increased inflammation and inclination to permanent liver damage. Given the limited treatment options available to patients, models that recapitulate critical features of disease pathogenesis are needed to improve drug development. Here, a MASLD model was developed by differentiating hepatocyte-like cells (HLCs) from human induced pluripotent stem cells (hiPSCs) in 2D and 3D, in which hepatic aggregates exhibited enhanced functionality. Induced HLCs exposed to free fatty acids led to a steatotic phenotype, partially reducing hepatic function. Biochemical cues released from induced HLCs promoted activation of fibroblasts, resulting in increased inflammatory cytokine secretion and extracellular matrix (ECM) deposition. These findings suggest paracrine signaling from hepatocytes to the surrounding stroma can trigger the progression of MASH and fibrosis. Collectively, our results demonstrate the utility of hiPSC derivatives for modeling liver diseases and reveal how heterotypic interactions can drive disease progression.

Indexed as

Fatty LiverHepatocytesInduced Pluripotent Stem CellsModels, BiologicalCell DifferentiationCells, CulturedCytokinesDisease ProgressionExtracellular MatrixFibroblastsHumansCytokines

Identifiers

PMID41501149
PMCPMC12873437

What Socratic 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 Socratic graph.