Evidence map›Paper›PMID 40158856›Full record

ArticleThe Journal of biological chemistry2025

Activating transcription factor 3 regulates hepatic apolipoprotein A4 upon metabolic stress.

Jasmine Encarnacion, Danielle M Smith, Joseph Choi, Joseph Scafidi, Michael J Wolfgang

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of biological chemistry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. Article
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

5 authors.

Jasmine EncarnacionDepartment of Physiology, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA; Department of Pharmacology and Molecular Sciences, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Danielle M SmithDepartment of Biological Chemistry, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Joseph ChoiDepartment of Biological Chemistry, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Joseph ScafidiDepartment of Neurology, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA; The Michael V. Johnston Center for Developmental Neuroscience, Kennedy Krieger Institute, Baltimore, Maryland, USA.
Michael J WolfgangDepartment of Physiology, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA; Department of Pharmacology and Molecular Sciences, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA; Department of Biological Chemistry, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. Electronic address: mwolfga1@jhmi.edu.

Funding

Pharmacology and Molecular Sciences Training Program: Enhancing Inclusivity Through Universal Design for Learning in Graduate CoursesT32GM135083 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI Caren L. Freel Meyers · 2020 to 2026
$3.3M
Coordination of hepatic fatty acid metabolismR01DK120530 · NIDDK · JOHNS HOPKINS UNIVERSITY · PI WOLFGANG, MICHAEL J. · 2020 to 2024
$2.0M
Coordination of fatty acid metabolism following neonatal brain injury from preterm birthR01NS125653 · NINDS · HUGO W. MOSER RES INST KENNEDY KRIEGER · PI Joseph Scafidi, Susanna Scafidi · 2022 to 2026
$1.9M
Novel roles of hepatic fatty acid oxidationR56DK138507 · NIDDK · JOHNS HOPKINS UNIVERSITY · PI WOLFGANG, MICHAEL J. · 2024 to 2024
$409k
NIDDK NIH HHS R01 DK120530NIDDK NIH HHS R56 DK138507NIGMS NIH HHS T32 GM135083NINDS NIH HHS R01 NS125653
6 · The paper itself

Abstract

The liver plays essential roles in maintaining systemic glucolipid homeostasis under ever changing metabolic stressors. Metabolic dysregulation can lead to both adaptive and maladaptive changes that impact systemic physiology. Here, we examined disparate genetic and environmental metabolic stressors and identified apolipoprotein A4 (ApoA4) as a circulating protein upregulated in liver-specific KOs for carnitine palmitoyltransferase 2 and pyruvate carboxylase. We found this upregulation to be exacerbated by fasting and high-fat or ketogenic diets. Unique among these models was a concomitant increase in activating transcription factor 3 (Atf3). Liver-specific overexpression of Atf3 resulted in increased ApoA4 expression in a sex-dependent manner. To understand the requirement of Atf3 to metabolic stress, we generated liver-specific Atf3, Cpt2 double KO mice. These experiments demonstrated the requirement for Atf3 in the induction of ApoA4 mRNA, ApoA4 protein, and serum triglycerides that were also sex-dependent. These experiments reveal the roles of hepatic Atf3 and ApoA4 in response to metabolic stress in vivo.

Indexed as

Activating Transcription Factor 3Apolipoproteins ALiverStress, PhysiologicalAnimalsCarnitine O-PalmitoyltransferaseFemaleMaleMiceMice, Inbred C57BLMice, KnockoutTriglyceridesActivating Transcription Factor 3apolipoprotein A-IVApolipoproteins AAtf3 protein, mouseCarnitine O-PalmitoyltransferaseTriglyceridesapolipoprotein A4Atf3fatty acid oxidationgene knockoutliver metabolismmetabolic regulationsex-dependenttranscription factor

Identifiers

PMID40158856
PMCPMC12059330

What OpenQuestion holds

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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.