Evidence map›Paper›PMID 29335425›Full record

ArticleScientific reports2018

SPARC expression is associated with hepatic injury in rodents and humans with non-alcoholic fatty liver disease.

Guillermo Mazzolini, Catalina Atorrasagasti, Agostina Onorato, Estanislao Peixoto, Martin Schlattjan, Jan-Peter Sowa, Svenja Sydor, Guido Gerken, Ali Canbay

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

20 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
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  3. Immunonutrition: Another Player on the MASLD Field.International journal of molecular sciences · 2025
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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

9 authors at 3 institutions in 2 countries.

Guillermo MazzoliniGene Therapy Laboratory, Instituto de Investigaciones en Medicina Traslacional, Universidad Austral, Buenos Aires, Argentina.
Catalina AtorrasagastiGene Therapy Laboratory, Instituto de Investigaciones en Medicina Traslacional, Universidad Austral, Buenos Aires, Argentina.
Agostina OnoratoGene Therapy Laboratory, Instituto de Investigaciones en Medicina Traslacional, Universidad Austral, Buenos Aires, Argentina.
Estanislao PeixotoGene Therapy Laboratory, Instituto de Investigaciones en Medicina Traslacional, Universidad Austral, Buenos Aires, Argentina.
Martin SchlattjanDepartment for Gastroenterology and Hepatology, University Hospital, University Duisburg-Essen, Essen, Germany.
Jan-Peter SowaDepartment for Gastroenterology and Hepatology, University Hospital, University Duisburg-Essen, Essen, Germany.
Svenja SydorDepartment for Gastroenterology and Hepatology, University Hospital, University Duisburg-Essen, Essen, Germany.
Guido GerkenDepartment for Gastroenterology and Hepatology, University Hospital, University Duisburg-Essen, Essen, Germany.
Ali CanbayDepartment for Gastroenterology and Hepatology, University Hospital, University Duisburg-Essen, Essen, Germany. ali.canbay@med.ovgu.de.
University of Duisburg-Essen · DEAustral University · ARConsejo Nacional de Investigaciones Científicas y Técnicas · AR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mechanisms that control progression from simple steatosis to steato-hepatitis and fibrosis in patients with non-alcoholic fatty liver disease (NAFLD) are unknown. SPARC, a secreted matricellular protein, is over-expressed in the liver under chronic injury. Contribution of SPARC accumulation to disease severity is largely unknown in NAFLD. We assessed the hypothesis that SPARC is increased in livers with more necrosis and inflammation and could be associated with more fibrosis. qrt-PCR, immunohistochemistry, and ELISA were employed to localize and quantify changes in SPARC in 62 morbidly obese patients with NAFLD/NASH and in a mouse model of diet-induced-NASH. Results were correlated with the severity of NAFLD/NASH. In obese patients 2 subgroups were identified with either high SPARC expression (n = 16) or low SPARC expression (n = 46) in the liver, with a cutoff of 1.2 fold expression. High expression of SPARC paralleled hepatocellular damage and increased mRNA expression of pro-fibrogenic factors in the liver. In line with these findings, in the NASH animal model SPARC knockout mice were protected from inflammatory injury, and showed less inflammation and fibrosis. Hepatic SPARC expression is associated with liver injury and fibrogenic processes in NAFLD. SPARC has potential as preventive or therapeutic target in NAFLD patients.

Indexed as

AnimalsDisease Models, AnimalEnzyme-Linked Immunosorbent AssayFemaleHumansImmunohistochemistryMaleMice, KnockoutMiddle AgedNon-alcoholic Fatty Liver DiseaseOsteonectinReal-Time Polymerase Chain ReactionReverse Transcriptase Polymerase Chain ReactionOsteonectinSPARC protein, humanSPARC protein, mouse

Identifiers

PMID29335425
PMCPMC5768809
OpenAlexW2782796034

What OpenQuestion holds

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Registered trials

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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.