Evidence map›Paper›PMID 30011790›Full record

ReviewInternational journal of molecular sciences2018

New Aspects of Lipotoxicity in Nonalcoholic Steatohepatitis.

Nahum Mendez-Sanchez, Vania Cesar Cruz-Ramon, Oscar Lenin Ramirez-Perez, Jessica P Hwang, Beatriz Barranco-Fragoso, Jaqueline Cordova-Gallardo

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers.

0numbers the graph read from it
0cells of the map it votes in
92citing papers in PubMed
13.1field-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

92 citing papers in PubMed, 175 citations in OpenAlex.

  1. Trial
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  3. Review
  4. Molecular medicine reports · 2026
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  8. Article
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  16. Article
  17. Article
  18. From Liver to Brain: How MAFLD/MASLD Impacts Cognitive Function.Medical science monitor : international medical journal of experimental and clinical research · 2024
    Review
  19. Review
  20. Review

32 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

6 authors at 4 institutions in 2 countries.

Nahum Mendez-SanchezLiver Research Unit, Medica Sur Clinic & Foundation, 14050 Mexico City, Mexico. nmendez@medicasur.org.mx.ORCID 0000-0001-5257-8048
Vania Cesar Cruz-RamonLiver Research Unit, Medica Sur Clinic & Foundation, 14050 Mexico City, Mexico. vaniacesar_ram55@hotmail.com.ORCID 0000-0002-5149-9636
Oscar Lenin Ramirez-PerezLiver Research Unit, Medica Sur Clinic & Foundation, 14050 Mexico City, Mexico. oscar.tuzos@hotmail.com.ORCID 0000-0002-5808-3705
Jessica P HwangDepartment of General Internal Medicine, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA. jphwang@mdanderson.org.
Beatriz Barranco-FragosoDepartment of Gastroenterology, National Medical Center "20 Noviembre", 03229 Mexico City, Mexico. betbarranco@yahoo.com.mx.
Jaqueline Cordova-GallardoObesity Clinic, General Hospital "Dr. Manuel Gea González", 14080 Mexico City, Mexico. jacquiemex2@yahoo.com.mx.
Hospital Médica Sur · MXHospital General Dr. Manuel Gea Gonzalez · MXInstitute for Social Security and Services for State Workers · MXThe University of Texas MD Anderson Cancer Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

NASH is becoming increasingly common worldwide because of the growing global prevalence of obesity and consequently NAFLD. Unfortunately, the mechanism of progression of NAFLD to NASH and then cirrhosis is not completely understood. Several factors, including insulin resistance, inflammation, oxidative stress, lipotoxicity, and bile acid (BA) toxicity, have been reported to be associated with NASH progression. The release of fatty acids from dysfunctional and insulin-resistant adipocytes results in lipotoxicity, which is caused by the ectopic accumulation of triglyceride-derived toxic metabolites and the subsequent activation of inflammatory pathways, cellular dysfunction, and lipoapoptosis. Adipose tissue (AT), especially visceral AT, comprises multiple cell populations that produce adipokines and insulin-like growth factor, plus macrophages and other immune cells that stimulate the development of lipotoxic liver disease. These biomolecules have been recently linked with many digestive diseases and gastrointestinal malignancies such as hepatocellular carcinoma. This made us question what role lipotoxicity has in the natural history of liver fibrosis. Therefore, this review focuses on the close relationship between AT and NASH. A good comprehension of the pathways that are related to dysregulated AT, metabolic dysfunction, and hepatic lipotoxicity will result in the development of prevention strategies and promising therapeutics for patients with NASH.

Indexed as

AdipokinesAdipose TissueDisease ProgressionFatty AcidsHumansInsulin ResistanceLiverLiver CirrhosisModels, BiologicalNon-alcoholic Fatty Liver DiseaseAdipokinesFatty Acidshepatic lipotoxicityliver fibrosisnonalcoholic steatohepatitis

Identifiers

PMID30011790
PMCPMC6073816
OpenAlexW2884913483

What OpenQuestion 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 OpenQuestion graph.