Evidence map›Paper›PMID 26912150›Full record

ReviewDiabetes & metabolism journal2016

Novel Molecular Mechanisms in the Development of Non-Alcoholic Steatohepatitis.

Davide Povero, Ariel E Feldstein

Open access · goldAbstract readReview
In one paragraph

Review in Diabetes & metabolism journal, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
8.1field-weighted citation impact, top 2% 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

30 citing papers in PubMed, 1 synthesis or guideline pooled it, 60 citations in OpenAlex.

  1. Relationship between prevalence and risk of osteoporosis or osteoporotic fracture with non-alcoholic fatty liver disease: A systematic review and meta-analysis.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2022
    Pooled it
  2. Review
  3. AMPK-Targeting Effects of (-)-Epicatechin Gallate fromInternational journal of molecular sciences · 2025
    Article
  4. Exogenous HScientific reports · 2025
    Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Lipid mediators of liver injury in nonalcoholic fatty liver disease.American journal of physiology. Gastrointestinal and liver physiology · 2019
    Review
  17. Article
  18. Review
  19. Apoptosis and non-alcoholic fatty liver diseases.World journal of gastroenterology · 2018
    Review
  20. Article
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

2 authors at 1 institution in 1 country.

Davide PoveroDivision of Gastroenterology, Hepatology and Nutrition, Department of Pediatrics, Rady's Children Hospital, University of California San Diego, San Diego, CA, USA.
Ariel E FeldsteinDivision of Gastroenterology, Hepatology and Nutrition, Department of Pediatrics, Rady's Children Hospital, University of California San Diego, San Diego, CA, USA. afeldstein@ucsd.edu.ORCID http://orcid.org/0000-0001-7202-3840
University of California San Diego · US

Funding

Oxidized Metabolites of Linoleic Acid in Alcohol-induced Liver InjuryU01AA022489 · NIAAA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI FELDSTEIN, ARIEL, MCCLAIN, CRAIG J. · 2014 to 2018
$1.7M
Encapsulated RNAs in extracellular vesicles contribute ALD progressionR21AA023574 · NIAAA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI EGUCHI, AKIKO, FELDSTEIN, ARIEL · 2015 to 2016
$407k
NIAAA NIH HHS R21 AA023574NIAAA NIH HHS U01 AA022489
6 · The paper itself

Abstract

Non-alcoholic fatty liver disease (NAFLD) is one of the most common causes of chronic liver disease in adults and children worldwide. NAFLD has become a severe health issue and it can progress towards a more severe form of the disease, the non-alcoholic steatohepatitis (NASH). A combination of environmental factors, host genetics, and gut microbiota leads to excessive accumulation of lipids in the liver (steatosis), which may result in lipotoxicity and trigger hepatocyte cell death, liver inflammation, fibrosis, and pathological angiogenesis. NASH can further progress towards liver cirrhosis and cancer. Over the last few years, cell-derived extracellular vesicles (EVs) have been identified as effective cell-to-cell messengers that transfer several bioactive molecules in target cells, modulating the pathogenesis and progression of NASH. In this review, we focused on recently highlighted aspects of molecular pathogenesis of NASH, mediated by EVs via their bioactive components. The studies included in this review summarize the state of art regarding the role of EVs during the progression of NASH and bring novel insight about the potential use of EVs for diagnosis and therapeutic strategies for patients with this disease.

Indexed as

AngiogenesisCell deathCirrhosisExtracellular vesiclesLipotoxicity

Identifiers

PMID26912150
PMCPMC4768045
OpenAlexW2278549513

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.