Evidence map›Paper›PMID 36300120›Full record

ReviewFrontiers in immunology2022

The immune response as a therapeutic target in non-alcoholic fatty liver disease.

Nicolás Ortiz-López, Catalina Fuenzalida, María Soledad Dufeu, Araceli Pinto-León, Alejandro Escobar, Jaime Poniachik, Juan Pablo Roblero, Lucía Valenzuela-Pérez, Caroll J Beltrán

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
3.9field-weighted citation impact, top 5% 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

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.

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  15. Current strategies for nonalcoholic fatty liver disease treatment (Review).International journal of molecular medicine · 2024
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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 2 institutions in 1 country.

Nicolás Ortiz-LópezLaboratory of Immunogastroenterology, Unit of Gastroenterology, Department of Medicine, Hospital Clínico Universidad de Chile, Santiago, Chile.
Catalina FuenzalidaLaboratory of Immunogastroenterology, Unit of Gastroenterology, Department of Medicine, Hospital Clínico Universidad de Chile, Santiago, Chile.
María Soledad DufeuLaboratory of Immunogastroenterology, Unit of Gastroenterology, Department of Medicine, Hospital Clínico Universidad de Chile, Santiago, Chile.
Araceli Pinto-LeónLaboratory of Immunogastroenterology, Unit of Gastroenterology, Department of Medicine, Hospital Clínico Universidad de Chile, Santiago, Chile.
Alejandro EscobarFaculty of Dentistry, Universidad de Chile, Santiago, Chile.
Jaime PoniachikUnit of Gastroenterology, Department of Medicine, Hospital Clínico Universidad de Chile, Santiago, Chile.
Juan Pablo RobleroUnit of Gastroenterology, Department of Medicine, Hospital Clínico Universidad de Chile, Santiago, Chile.
Lucía Valenzuela-PérezLaboratory of Immunogastroenterology, Unit of Gastroenterology, Department of Medicine, Hospital Clínico Universidad de Chile, Santiago, Chile.
Caroll J BeltránLaboratory of Immunogastroenterology, Unit of Gastroenterology, Department of Medicine, Hospital Clínico Universidad de Chile, Santiago, Chile.
Hospital Clínico de la Universidad de Chile · CLUniversity of Chile · CL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Non-alcoholic fatty liver disease (NAFLD) is a complex and heterogeneous disorder considered a liver-damaging manifestation of metabolic syndrome. Its prevalence has increased in the last decades due to modern-day lifestyle factors associated with overweight and obesity, making it a relevant public health problem worldwide. The clinical progression of NAFLD is associated with advanced forms of liver injury such as fibrosis, cirrhosis, and hepatocellular carcinoma (HCC). As such, diverse pharmacological strategies have been implemented over the last few years, principally focused on metabolic pathways involved in NAFLD progression. However, a variable response rate has been observed in NAFLD patients, which is explained by the interindividual heterogeneity of susceptibility to liver damage. In this scenario, it is necessary to search for different therapeutic approaches. It is worth noting that chronic low-grade inflammation constitutes a central mechanism in the pathogenesis and progression of NAFLD, associated with abnormal composition of the intestinal microbiota, increased lymphocyte activation in the intestine and immune effector mechanisms in liver. This review aims to discuss the current knowledge about the role of the immune response in NAFLD development. We have focused mainly on the impact of altered gut-liver-microbiota axis communication on immune cell activation in the intestinal mucosa and the role of subsequent lymphocyte homing to the liver in NAFLD development. We further discuss novel clinical trials that addressed the control of the liver and intestinal immune response to complement current NAFLD therapies.

Indexed as

Carcinoma, HepatocellularLiver NeoplasmsNon-alcoholic Fatty Liver DiseaseFibrosisHumansImmunityliver diseasesliver fibrosisliver lymphocyte hominglow-grade inflammationmicrobiotamicrobiota-gut-liver axisnon-alcoholic fatty liver disease (NAFLD)steatohepatitis (NASH)

Identifiers

PMID36300120
PMCPMC9589255
OpenAlexW4304144157

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.