Evidence map›Paper›PMID 28068223›Full record

ArticleCell metabolism2016

Hepatocyte TAZ/WWTR1 Promotes Inflammation and Fibrosis in Nonalcoholic Steatohepatitis.

Xiaobo Wang, Ze Zheng, Jorge Matias Caviglia, Kathleen E Corey, Tina M Herfel, Bishuang Cai, Ricard Masia, Raymond T Chung, Jay H Lefkowitch, Robert F Schwabe and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell metabolism, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 245 papers.

0numbers the graph read from it
0cells of the map it votes in
245citing papers in PubMed
14.1field-weighted citation impact, top 1% of its field
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

245 citing papers in PubMed, 398 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Mechanisms and therapeutic insights into MASH-associated fibrosis.Trends in endocrinology and metabolism: TEM · 2026
    Review
  9. Review
  10. Macrophage β-catenin-Ihh axis induces hepatic stellate cell activation and fibrosis in metabolic dysfunction-associated steatohepatitis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Article
  11. Article
  12. Article
  13. Article
  14. Genetic Predisposition to MASLD: Potential for Therapeutic Management.International journal of molecular sciences · 2026
    Review
  15. Review
  16. Article
  17. Review
  18. Molecular mechanisms in MASLD/MASH-related HCC.Hepatology (Baltimore, Md.) · 2025
    Review
  19. Article
  20. Article

185 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 3 institutions in 1 country.

Xiaobo WangDepartment of Medicine, Columbia University, New York, NY 10032, USA. Electronic address: xw2279@columbia.edu.
Ze ZhengDepartment of Medicine, Columbia University, New York, NY 10032, USA.
Jorge Matias CavigliaDepartment of Medicine, Columbia University, New York, NY 10032, USA; Institute of Human Nutrition, Columbia University, New York, NY 10032, USA.
Kathleen E CoreyGastrointestinal Unit, Massachusetts General Hospital, Boston, MA, 02114, USA; Harvard Medical School, Boston, MA 02115, USA.
Tina M HerfelTeklad Diets, Envigo, Madison, WI, 53713, USA.
Bishuang CaiDepartment of Medicine, Columbia University, New York, NY 10032, USA.
Ricard MasiaHarvard Medical School, Boston, MA 02115, USA; Department of Pathology and Laboratory Medicine, Massachusetts General Hospital, Boston, MA, 02114, USA.
Raymond T ChungGastrointestinal Unit, Massachusetts General Hospital, Boston, MA, 02114, USA; Harvard Medical School, Boston, MA 02115, USA.
Jay H LefkowitchDepartment of Pathology and Cell Biology, Columbia University, New York, NY 10032, USA.
Robert F SchwabeDepartment of Medicine, Columbia University, New York, NY 10032, USA; Institute of Human Nutrition, Columbia University, New York, NY 10032, USA.
Ira TabasDepartment of Medicine, Columbia University, New York, NY 10032, USA; Department of Pathology and Cell Biology, Columbia University, New York, NY 10032, USA; Department of Physiology and Cellular Biophysics, Columbia University, New York, NY 10032, USA. Electronic address: iat1@columbia.edu.
Columbia University · USMassachusetts General Hospital · USHarvard University · US

Funding

RESEARCH TRAININGP30DK026687 · NIDDK · ST. LUKE'S-ROOSEVELT INST FOR HLTH SCIS · PI Anthony W Ferrante, DYMPNA GALLAGHER · 1986 to 2026
$33.0M
TTC39B in obesity and atherosclerosisP01HL087123 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI WANG, NAN · 2007 to 2022
$31.2M
Clinical and Translational Science AwardUL1TR000040 · NCATS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI GINSBERG, HENRY N · 2012 to 2015
$26.2M
The Unfolded Protein Response in Sterol CytoxicityR01HL075662 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI TABAS, IRA A · 2004 to 2017
$5.6M
Enhancing Inflammation Resolution in Atherosclerosis via Targeted Nanoparticle-Mediated Delivery of BiologicsR01HL127464 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI SHI, JINJUN, TABAS, IRA A · 2016 to 2019
$3.0M
Patient-Oriented Research on Hepatitis in Special PopulationsK24DK078772 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI CHUNG, RAYMOND T · 2007 to 2016
$1.6M
The Impact of Obstructive Sleep Apnea on Non-Alcoholic Fatty Liver DiseaseK23DK099422 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI COREY, KATHLEEN ELIZABETH · 2013 to 2017
$938k
TLR4 in Obesity-Driven Liver FibrosisR03DK101863 · NIDDK · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI CAVIGLIA, JORGE MATIAS · 2014 to 2016
$600k
TLR4 in obesity-driven liver cancerK22CA178098 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI CAVIGLIA, JORGE MATIAS · 2013 to 2015
$391k
NCATS NIH HHS UL1 TR000040NCI NIH HHS K22 CA178098NHLBI NIH HHS P01 HL087123NHLBI NIH HHS R01 HL075662NHLBI NIH HHS R01 HL127464NIDDK NIH HHS K23 DK099422NIDDK NIH HHS K24 DK078772NIDDK NIH HHS P30 DK026687NIDDK NIH HHS R03 DK101863
6 · The paper itself

Abstract

Nonalcoholic steatohepatitis (NASH) is a leading cause of liver disease worldwide. However, the molecular basis of how benign steatosis progresses to NASH is incompletely understood, which has limited the identification of therapeutic targets. Here we show that the transcription regulator TAZ (WWTR1) is markedly higher in hepatocytes in human and murine NASH liver than in normal or steatotic liver. Most importantly, silencing of hepatocyte TAZ in murine models of NASH prevented or reversed hepatic inflammation, hepatocyte death, and fibrosis, but not steatosis. Moreover, hepatocyte-targeted expression of TAZ in a model of steatosis promoted NASH features, including fibrosis. In vitro and in vivo mechanistic studies revealed that a key mechanism linking hepatocyte TAZ to NASH fibrosis is TAZ/TEA domain (TEAD)-mediated induction of Indian hedgehog (Ihh), a secretory factor that activates fibrogenic genes in hepatic stellate cells. In summary, TAZ represents a previously unrecognized factor that contributes to the critical process of steatosis-to-NASH progression.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsBase SequenceCell DeathDietDisease Models, AnimalDisease ProgressionGene SilencingHedgehog ProteinsHepatic Stellate CellsHepatocytesHumansInflammationIntracellular Signaling Peptides and ProteinsLiverLiver CirrhosisAdaptor Proteins, Signal TransducingHedgehog ProteinsIntracellular Signaling Peptides and ProteinsTrans-ActivatorsTranscriptional Coactivator with PDZ-Binding Motif ProteinsTranscription FactorsWWTR1 protein, humanWwtr1 protein, mouse

Identifiers

PMID28068223
PMCPMC5226184
OpenAlexW2541359632

What OpenQuestion holds

Textmetadata
LicenceTDM
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 OpenQuestion graph.