Evidence map›Paper›PMID 25892859›Full record

ReviewWorld journal of gastroenterology2015

Nonalcoholic fatty liver disease, metabolic risk factors, and hepatocellular carcinoma: an open question.

Letiția Adela Maria Streba, Cristin Constantin Vere, Ion Rogoveanu, Costin Teodor Streba

Open access · hybridAbstract readEditorialReview
In one paragraph

Review in World journal of gastroenterology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
85citing papers in PubMed, 1 pooled it
10.5field-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

85 citing papers in PubMed, 1 synthesis or guideline pooled it, 159 citations in OpenAlex.

  1. Pooled it
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  7. Deregulated miR-487b-3p in Patients with Non-Alcoholic Fatty Liver Disease and Its Regulatory Effect on Insulin Resistance.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2026
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25 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

4 authors at 1 institution in 1 country.

Letiția Adela Maria StrebaLetiția Adela Maria Streba, Internal Medicine, Medical Semiology, University of Medicine and Pharmacy of Craiova, 200639 Craiova, Romania.
Cristin Constantin VereLetiția Adela Maria Streba, Internal Medicine, Medical Semiology, University of Medicine and Pharmacy of Craiova, 200639 Craiova, Romania.
Ion RogoveanuLetiția Adela Maria Streba, Internal Medicine, Medical Semiology, University of Medicine and Pharmacy of Craiova, 200639 Craiova, Romania.
Costin Teodor StrebaLetiția Adela Maria Streba, Internal Medicine, Medical Semiology, University of Medicine and Pharmacy of Craiova, 200639 Craiova, Romania.
University of Medicine and Pharmacy of Craiova · RO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Non-alcoholic liver disease (NAFLD) defines liver abnormalities ranging from simple steatosis to nonalcoholic steatohepatitis with or without cirrhosis development, occurring in the absence of significant alcohol consumption, use of teratogenic medication, or hereditary disorders. The association between NAFLD and metabolic syndrome is well documented and widely recognized. Obesity, type 2 diabetes mellitus (T2DM), and dyslipidemia are the most common metabolic risk factors associated with NAFLD. Among the components of metabolic syndrome, current evidence strongly indicates obesity and diabetes as hepatocellular carcinoma (HCC) risk factors. There is also growing evidence that suggests an increased risk of HCC in NAFLD patients, even surpassing other etiologies in some high-income countries. Epidemiologic data demonstrate a parallel rise in prevalence of obesity, diabetes, NAFLD, and HCC. As obesity and its related diseases have steadily afflicted larger populations, HCC incidence is expected to increase in the future. Pathophysiologic mechanisms that underlie NAFLD development and subsequent progression to nonalcoholic steatohepatitis and cirrhosis (insulin resistance and hyperinsulinemia, oxidative stress, hepatic stellate cell activation, cytokine/adipocytokine signaling pathways, and genetic and environmental factors) appear to play a significant role in the development of NAFLD-related HCC. However, a comprehensive view of molecular mechanisms linking obesity, T2DM, and NAFLD-related HCC, as well as the exact sequence of molecular events, is still not understood in its entirety. Good-quality data are still necessary, and efforts should continue towards better understanding the underlying carcinogenic mechanisms of NAFLD-related HCC. In this paper, we aimed to centralize the most important links supporting these relationships, focusing on obesity, T2DM, and NAFLD-related HCC, as well as point out the major gaps in knowledge regarding the underlying molecular mechanisms behind them.

Indexed as

AnimalsCarcinoma, HepatocellularDiabetes Mellitus, Type 2Disease Models, AnimalDisease ProgressionHumansLiver CirrhosisLiver NeoplasmsMetabolic SyndromeNon-alcoholic Fatty Liver DiseaseObesityPrognosisRisk AssessmentRisk FactorsDiabetes mellitusHepatocellular carcinomaMetabolic syndromeNon-alcoholic fatty liver diseaseObesity

Identifiers

PMID25892859
PMCPMC4394070
OpenAlexW2062336519

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.