Evidence map›Paper›PMID 22570745›Full record

ArticleGut and liver2012

NASH is an Inflammatory Disorder: Pathogenic, Prognostic and Therapeutic Implications.

Geoffrey C Farrell, Derrick van Rooyen, Lay Gan, Shivrakumar Chitturi

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Gut and liver, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 187 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
187citing papers in PubMed, 3 pooled it
18.9field-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

187 citing papers in PubMed, 3 syntheses or guidelines pooled it, 393 citations in OpenAlex.

  1. Pooled it
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  10. Fermented Milk as an Alternative Therapy for Obesity.International journal of food science · 2026
    Review
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  17. ACS pharmacology & translational science · 2025
    Article
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127 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 2 institutions in 1 country.

Geoffrey C FarrellGastroenterology and Hepatology Unit, The Canberra Hospital, Australian National University Medical School, Garran, Australia.
Derrick van Rooyen
Lay Gan
Shivrakumar Chitturi
Australian National University · AUCanberra Hospital · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

While non-alcoholic fatty liver disease (NAFLD) is highly prevalent (15% to 45%) in modern societies, only 10% to 25% of cases develop hepatic fibrosis leading to cirrhosis, end-stage liver disease or hepatocellular carcinoma. Apart from pre-existing fibrosis, the strongest predictor of fibrotic progression in NAFLD is steatohepatitis or non-alcoholic steatohepatitis (NASH). The critical features other than steatosis are hepatocellular degeneration (ballooning, Mallory hyaline) and mixed inflammatory cell infiltration. While much is understood about the relationship of steatosis to metabolic factors (over-nutrition, insulin resistance, hyperglycemia, metabolic syndrome, hypoadiponectinemia), less is known about inflammatory recruitment, despite its importance for the perpetuation of liver injury and fibrogenesis. In this review, we present evidence that liver inflammation has prognostic significance in NAFLD. We then consider the origins and components of liver inflammation in NASH. Hepatocytes injured by toxic lipid molecules (lipotoxicity) play a central role in the recruitment of innate immunity involving Toll-like receptors (TLRs), Kupffer cells (KCs), lymphocytes and neutrophils and possibly inflammasome. The key pro-inflammatory signaling pathways in NASH are nuclear factor-kappa B (NF-κB) and c-Jun N-terminal kinase (JNK). The downstream effectors include adhesion molecules, chemokines, cytokines and the activation of cell death pathways leading to apoptosis. The upstream activators of NF-κB and JNK are more contentious and may depend on the experimental model used. TLRs are strong contenders. It remains possible that inflammation in NASH originates outside the liver and in the gut microbiota that prime KC/TLR responses, inflamed adipose tissue and circulating inflammatory cells. We briefly review these mechanistic considerations and project their implications for the effective treatment of NASH.

Indexed as

Hepatic fibrosisNon-alcoholic fatty liver diseaseNon-alcoholic steatohepatitis

Identifiers

PMID22570745
PMCPMC3343154
OpenAlexW2084589154

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.