Evidence map›Paper›PMID 25873773›Full record

ReviewMediators of inflammation2015

OSAS-related inflammatory mechanisms of liver injury in nonalcoholic fatty liver disease.

Elena Paschetta, Paola Belci, Anna Alisi, Daniela Liccardo, Renato Cutrera, Giovanni Musso, Valerio Nobili

Open access · goldAbstract readReview
In one paragraph

Review in Mediators of inflammation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 3 pooled it
3.5field-weighted citation impact, top 7% 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, 3 syntheses or guidelines pooled it, 51 citations in OpenAlex.

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  8. [Metabolic-associated fatty liver disease (MAFLD): a multisystemic disease beyond the liver].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 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

7 authors at 2 institutions in 1 country.

Elena PaschettaGradenigo Hospital, University of Turin, Corso Regina Margherita, 10132 Turin, Italy.
Paola BelciDepartment of Medical Sciences, San Giovanni Battista Hospital, University of Turin, Corso Bramante 14, 10124 Turin, Italy.
Anna AlisiHepato-Metabolic Disease Unit, Bambino Gesù Children's Hospital and IRCCS, S. Onofrio Square 4, 00165 Rome, Italy.
Daniela LiccardoHepato-Metabolic Disease Unit, Bambino Gesù Children's Hospital and IRCCS, S. Onofrio Square 4, 00165 Rome, Italy.
Renato CutreraPneumology Unit, Sleep and Noninvasive Ventilation Laboratory, Bambino Gesù Children's Hospital and IRCCS, S. Onofrio Square 4, 00165 Rome, Italy.
Giovanni MussoGradenigo Hospital, University of Turin, Corso Regina Margherita, 10132 Turin, Italy.ORCID 0000-0002-8569-2872
Valerio NobiliHepato-Metabolic Disease Unit, Bambino Gesù Children's Hospital and IRCCS, S. Onofrio Square 4, 00165 Rome, Italy.
Bambino Gesù Children's Hospital · ITUniversity of Turin · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Obstructive sleep apnoea syndrome (OSAS) is a common sleep disorder, affecting over 4% of the general population, and is associated with metabolic syndrome and cardiovascular disease, independent of obesity and traditional risk factors. OSAS has been recently connected to nonalcoholic fatty liver disease (NAFLD), the most common chronic liver disease in the world, which can be found in 30% of the general adult population. Several studies suggest that the chronic intermittent hypoxia (CIH) of OSAS patients may per se trigger liver injury, inflammation, and fibrogenesis, promoting NAFLD development and the progression from steatosis to steatohepatitis, cirrhosis, and hepatocellular carcinoma. In NAFLD patients, liver disease may be caused by hypoxia both indirectly by promoting inflammation and insulin resistance and directly by enhancing proinflammatory cytokine production and metabolic dysregulation in liver cells. In this review, we focus on molecular mechanisms linking OSAS to NAFLD, including hypoxia inducible factor (HIF), nuclear factor kappa B (NF-κB), YKL-40, unfolded protein response, and hypoxic adipose tissue inflammation, which all could provide novel potential therapeutic approaches for the management of NAFLD patients with OSAS.

Indexed as

AdipokinesChitinase-3-Like Protein 1HumansHypoxiaHypoxia-Inducible Factor 1, alpha SubunitInflammationInsulin ResistanceLectinsNF-kappa BNon-alcoholic Fatty Liver DiseaseSleep Apnea, ObstructiveTumor Necrosis Factor-alphaUnfolded Protein ResponseAdipokinesCHI3L1 protein, humanChitinase-3-Like Protein 1Hypoxia-Inducible Factor 1, alpha SubunitLectinsNF-kappa BTumor Necrosis Factor-alpha

Identifiers

PMID25873773
PMCPMC4383458
OpenAlexW1994489206

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.