Evidence map›Paper›PMID 42244764›Full record

ArticlebioRxiv : the preprint server for biology2026

Hepatocyte TEAD1 drives epithelial-stromal remodeling during cholestatic liver injury.

Kumar Amit, Lee Jeongkyung, Negi Vinny, Mandi Varun, Filingeri Domenic, Danvers Joey, Pant Rajat, Ghosh Samit, Moulik Mousumi, Yechoor Vijay K

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PubMed Full text at PMC Publisher
In one paragraph

Article in bioRxiv : the preprint server for biology, 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

10 authors.

Kumar AmitDivision of Endocrinology, Diabetes & Metabolism, Department of Medicine, University of Pittsburgh, PA, USA.ORCID 0009-0001-6650-977X
Lee JeongkyungDivision of Endocrinology, Diabetes & Metabolism, Department of Medicine, University of Pittsburgh, PA, USA.ORCID 0000-0002-0260-7397
Negi VinnyDivision of Endocrinology, Diabetes & Metabolism, Department of Medicine, University of Pittsburgh, PA, USA.
Mandi VarunDivision of Endocrinology, Diabetes & Metabolism, Department of Medicine, University of Pittsburgh, PA, USA.
Filingeri DomenicDivision of Endocrinology, Diabetes & Metabolism, Department of Medicine, University of Pittsburgh, PA, USA.
Danvers JoeyDivision of Endocrinology, Diabetes & Metabolism, Department of Medicine, University of Pittsburgh, PA, USA.
Pant RajatDepartment of Medicine, Pittsburgh Heart, Lung, and Blood Vascular Medicine Institute, University of Pittsburgh, PA, USA.ORCID 0000-0003-3169-5151
Ghosh SamitDepartment of Medicine, Pittsburgh Heart, Lung, and Blood Vascular Medicine Institute, University of Pittsburgh, PA, USA.
Moulik MousumiDivision of Pediatric Cardiology, UPMC Children's Hospital of Pittsburgh, University of Pittsburgh, PA, USA.
Yechoor Vijay KDivision of Endocrinology, Diabetes & Metabolism, Department of Medicine, University of Pittsburgh, PA, USA.ORCID 0000-0002-9981-6784

Funding

Clock modulation in circadian desynchrony induced diabetes and atherovascular disease - mechanisms and interventionsR01DK128972 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI FIGUEIRO, MARIANA GROSS, PAUL, ANTONIO · 2021 to 2025
$3.7M
Circadian disruption-induced mitochondrial dysfunction in diabetesR01DK130499 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI YECHOOR, VIJAY K · 2021 to 2024
$1.8M
NIDDK NIH HHS R01 DK128972NIDDK NIH HHS R01 DK130499
6 · The paper itself

Abstract

Background & Aims: Primary sclerosing cholangitis (PSC) is a progressive cholangiopathy characterized by ductular remodeling, inflammation, and periportal fibrosis, for which effective medical therapies remain limited. The Hippo pathway effector TEAD1 has been implicated in liver regeneration and fibrogenesis; however, its role in cholestatic injury remains poorly defined. We investigated whether hepatocyte TEAD1 regulates injury-associated remodeling in a PSC-mimicking model and whether this mechanism is conserved in human PSC liver. Methods: Hepatocyte-specific TEAD1 knockout mice (Alb-TEAD1 Results: Hepatocyte TEAD1 deletion attenuated DDC-induced fibrosis, ductular expansion, and inflammatory cell accumulation, while preserving hepatocyte proliferative responses. TEAD1-deficient livers exhibited reduced expression of profibrotic mediators, including Conclusions: Hepatocyte TEAD1 drives ductular, inflammatory, and fibrogenic remodeling during cholestatic injury without disrupting bile acid metabolic adaptation. These findings identify TEAD1 as a hepatocyte-intrinsic regulator of epithelial-stromal crosstalk and establish conserved activation of this pathway in human PSC, supporting TEAD-directed signaling as a therapeutic target.

Identifiers

PMID42244764
PMCPMC13232097

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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.