Evidence map›Paper›PMID 41768523›Full record

ArticleGastro hep advances2026

Loss of Early Growth Response Protein 1 in the Liver Leads to Hepatic Lipid Accumulation Driven by an Imbalance Between Fatty Acid β-Oxidation and Oxidative Phosphorylation.

Cristy R C Verzijl, Dicky Struik, Albert Gerding, Roos E Eilers, Rachel E Thomas, Mirjam Koster, Miriam Langelaar-Makkinje, Marieke Smit, Nicolette Huijkman, Rick Havinga and 7 more

Abstract read
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Article in Gastro hep advances, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

17 authors.

Cristy R C VerzijlLaboratory of Pediatrics, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
Dicky StruikLaboratory of Pediatrics, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
Albert GerdingLaboratory of Pediatrics, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
Roos E EilersLaboratory of Pediatrics, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
Rachel E ThomasFaculty of Veterinary Medicine, Dutch Molecular Pathology Center, Utrecht University, Utrecht, The Netherlands.
Mirjam KosterLaboratory of Pediatrics, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
Miriam Langelaar-MakkinjeLaboratory of Pediatrics, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
Marieke SmitLaboratory of Pediatrics, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
Nicolette HuijkmanLaboratory of Pediatrics, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
Rick HavingaLaboratory of Pediatrics, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
Niels KloosterhuisLaboratory of Pediatrics, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
Vincent W BloksLaboratory of Pediatrics, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
Justina C WoltersLaboratory of Pediatrics, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
Jan Freark de BoerLaboratory of Pediatrics, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
Bart van de SluisLaboratory of Pediatrics, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
Barbara M BakkerLaboratory of Pediatrics, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
Johan W JonkerLaboratory of Pediatrics, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background and Aims: Metabolic-associated fatty liver disease is a worldwide health problem characterized by increased hepatic lipid accumulation, leading to conditions like steatohepatitis, cirrhosis, and liver cancer. Early growth response protein 1 ( Methods: Hepatocyte-specific EGR1-deficient male mice were generated using CRISPR/Cas9. Mice were maintained under chow-fed conditions or challenged with a high-fat diet (HFD). Hepatic lipid levels, zonation, and gene expression were analyzed. Oxygen consumption was measured in mouse and human hepatocytes. Results: After a HFD challenge, hepatic EGR1-deficient mice showed a significant increase in hepatic triglyceride levels. Transcriptome analysis revealed an upregulation of genes related to fatty acid oxidation and downregulation of mitochondrial respiration genes in livers of both chow and HFD hepatic EGR1-deficient mice. Functional analysis showed reduced maximum oxygen consumption in EGR1-deficient mouse and human hepatocytes. Fasting-induced hepatic lipid accumulation indeed indicated reduced fatty acid oxidation efficiency upon ablation of EGR1. Conclusion: Hepatic EGR1 deficiency significantly alters lipid metabolism and mitochondrial function, indicating a role of EGR1 in regulating the balance between mitochondrial fatty acid β-oxidation and respiration in the liver.

Indexed as

Early Growth Response Protein 1Fatty Acid OxidationMetabolic-Associated Fatty Liver DiseaseMitochondrial Function

Identifiers

PMID41768523
PMCPMC12938867

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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.