Evidence map›Paper›PMID 35508978›Full record

ArticleMolecular medicine (Cambridge, Mass.)2022

JNK1 and JNK3: divergent functions in hippocampal metabolic-cognitive function.

Oriol Busquets, Triana Espinosa-Jiménez, Miren Ettcheto, Jordi Olloquequi, Mònica Bulló, Eva Carro, José Luis Cantero, Gemma Casadesús, Jaume Folch, Ester Verdaguer and 2 more

Open access · goldAbstract read
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.4field-weighted citation impact, top 48% 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

4 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. Article
  3. The role of JNK signaling pathway in organ fibrosis.Journal of advanced research · 2025
    Review
  4. Review
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

12 authors at 5 institutions in 3 countries.

Oriol BusquetsDepartment of Pharmacology, Toxicology and Therapeutic Chemistry, Pharmacy and Food Sciences Faculty, University of Barcelona, 08028, Barcelona, Spain.
Triana Espinosa-JiménezDepartment of Pharmacology, Toxicology and Therapeutic Chemistry, Pharmacy and Food Sciences Faculty, University of Barcelona, 08028, Barcelona, Spain.
Miren EttchetoDepartment of Pharmacology, Toxicology and Therapeutic Chemistry, Pharmacy and Food Sciences Faculty, University of Barcelona, 08028, Barcelona, Spain.
Jordi OlloquequiLaboratory of Cellular and Molecular Pathology, Facultad de Ciencias de La Salud, Instituto de Ciencias Biomédicas, Universidad Autónoma de Chile, Talca, Chile.
Mònica BullóDepartment of Biochemistry and Biotechnology, Medicine and Health Sciences Faculty, University Rovira i Virgili, 43201, Reus, Spain.
Eva CarroNetwork Center for Biomedical Research in Neurodegenerative Diseases (CIBERNED), Madrid, Spain.
José Luis CanteroCentre for Biomedical Research of Neurodegenerative Diseases (CIBERNED), Instituto de Salud Carlos III, 28029, Madrid, Spain.
Gemma CasadesúsDepartment of Pharmacology & Therapeutics, College of Medicine, University of Florida, Gainesville, FL, 32610, USA.
Jaume FolchDepartment of Biochemistry and Biotechnology, Medicine and Health Sciences Faculty, University Rovira i Virgili, 43201, Reus, Spain.
Ester VerdaguerCentre for Biomedical Research of Neurodegenerative Diseases (CIBERNED), Instituto de Salud Carlos III, 28029, Madrid, Spain.
Carme AuladellCentre for Biomedical Research of Neurodegenerative Diseases (CIBERNED), Instituto de Salud Carlos III, 28029, Madrid, Spain.
Antoni CaminsDepartment of Pharmacology, Toxicology and Therapeutic Chemistry, Pharmacy and Food Sciences Faculty, University of Barcelona, 08028, Barcelona, Spain. camins@ub.edu.ORCID 0000-0002-1229-5956
Instituto de Salud Carlos III · ESAlbert Einstein College of Medicine · USBiomedical Research Networking Center on Neurodegenerative Diseases · ESUniversidad Autónoma de Chile · CLUniversity of Florida · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

aimThe appearance of alterations in normal metabolic activity has been increasingly considered a risk factor for the development of sporadic and late-onset neurodegenerative diseases. In this report, we induced chronic metabolic stress by feeding of a high-fat diet (HFD) in order to study its consequences in cognition. We also studied the effects of a loss of function of isoforms 1 and 3 of the c-Jun N-terminal Kinases (JNK), stress and cell death response elements.

methodsAnimals were fed either with conventional chow or with HFD, from their weaning until their sacrifice at 9 months. Before sacrifice, body weight, intraperitoneal glucose and insulin tolerance test (IP-GTT and IP‑ITT) were performed to evaluate peripheral biometrics. Additionally, cognitive behavioral tests and analysis of spine density were performed to assess cognitive function. Molecular studies were carried out to confirm the effects of metabolic stressors in the hippocampus relative to cognitive loss.

resultsOur studies demonstrated that HFD in Jnk3

conclusionsDownregulation of JNK3 does not seem to be a suitable target for the modulation of energetic-cognitive dysregulations while loss of function of JNK1 seems to promote a good metabolic-cognitive profile, just like resistance to the negative effects of chronic feeding with HFD.

Indexed as

HippocampusMitogen-Activated Protein Kinase 8AnimalsBody WeightCognitionDiet, High-FatInsulinMiceMice, Inbred C57BLInsulinMitogen-Activated Protein Kinase 8CognitionHigh-fat dietJNK1JNK3Metabolism

Identifiers

PMID35508978
PMCPMC9066854
OpenAlexW4225411490

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.