Evidence map›Paper›PMID 26894897›Full record

ReviewCellular and molecular life sciences : CMLS2016

Pathogenesis of nonalcoholic steatohepatitis.

Wensheng Liu, Robert D Baker, Tavleen Bhatia, Lixin Zhu, Susan S Baker

Open access · greenAbstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
102citing papers in PubMed, 1 pooled it
18.4field-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

102 citing papers in PubMed, 1 synthesis or guideline pooled it, 222 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Effects of crowberry (Food & nutrition research · 2026
    Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Frontiers in cardiovascular medicine · 2025
    Article
  16. Review
  17. Article
  18. Common Denominator of MASLD and Some Non-Communicable Diseases.Current issues in molecular biology · 2024
    Review
  19. Article
  20. Article

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

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

5 authors at 2 institutions in 1 country.

Wensheng LiuDepartment of Pediatrics, Digestive Diseases and Nutrition Center, Women and Children's Hospital of Buffalo, The State University of New York at Buffalo (SUNY Buffalo), 3435 Main Street, 422 BRB, Buffalo, NY, 14214, USA. wl11@buffalo.edu.
Robert D BakerDepartment of Pediatrics, Digestive Diseases and Nutrition Center, Women and Children's Hospital of Buffalo, The State University of New York at Buffalo (SUNY Buffalo), 3435 Main Street, 422 BRB, Buffalo, NY, 14214, USA.
Tavleen BhatiaDepartment of Pediatrics, Digestive Diseases and Nutrition Center, Women and Children's Hospital of Buffalo, The State University of New York at Buffalo (SUNY Buffalo), 3435 Main Street, 422 BRB, Buffalo, NY, 14214, USA.
Lixin ZhuDepartment of Pediatrics, Digestive Diseases and Nutrition Center, Women and Children's Hospital of Buffalo, The State University of New York at Buffalo (SUNY Buffalo), 3435 Main Street, 422 BRB, Buffalo, NY, 14214, USA.
Susan S BakerDepartment of Pediatrics, Digestive Diseases and Nutrition Center, Women and Children's Hospital of Buffalo, The State University of New York at Buffalo (SUNY Buffalo), 3435 Main Street, 422 BRB, Buffalo, NY, 14214, USA. sbaker@upa.chob.edu.
University at Buffalo, State University of New York · USWomen & Children's Hospital of Buffalo · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nonalcoholic steatohepatitis (NASH) is a severe form of nonalcoholic fatty liver disease and a risk factor for cirrhosis and hepatocellular carcinoma. The pathological features of NASH include steatosis, hepatocyte injury, inflammation, and various degrees of fibrosis. Steatosis reflects disordered lipid metabolism. Insulin resistance and excessive fatty acid influx to the liver are two important contributing factors. Steatosis is also likely associated with lipotoxicity and cellular stresses such as oxidative stress and endoplasmic reticulum stress, which result in hepatocyte injury. Inflammation and fibrosis are frequently triggered by various signals such as proinflammatory cytokines and chemokines, released by injuried hepatocytes and activated Kupffer cells. Although much progress has been made, the pathogenesis of NASH is not fully elucidated. The purpose of this review is to discuss the current understanding of NASH pathogenesis, mainly focusing on factors contributing to steatosis, hepatocyte injury, inflammation, and fibrosis.

Indexed as

Adipose TissueAnimalsApoptosisAutophagyCarcinoma, HepatocellularChemokinesCytokinesFatty AcidsFibrosisGastrointestinal MicrobiomeGenetic Predisposition to DiseaseHepatic Stellate CellsHepatocytesHumansInflammationInsulin ResistanceChemokinesCytokinesFatty AcidsLipopolysaccharidesTransforming Growth Factor betaApoptosisAutophagyGenetic predispositionGut microbiotaHepatic stellate cells

Identifiers

PMID26894897
PMCPMC11108381
OpenAlexW2277891177

What OpenQuestion holds

Textmetadata
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.