Evidence map›Paper›PMID 32686726›Full record

ArticleScientific reports2020

Chemokine C-C motif ligand 2 overexpression drives tissue-specific metabolic responses in the liver and muscle of mice.

Fedra Luciano-Mateo, Noemí Cabré, Salvador Fernández-Arroyo, Gerard Baiges-Gaya, Anna Hernández-Aguilera, Elisabet Rodríguez-Tomàs, Cristina Muñoz-Pinedo, Javier A Menéndez, Jordi Camps, Jorge Joven

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

22 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
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  5. Role of cellular senescence in hepatic diseases (Review).International journal of molecular medicine · 2025
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  7. Immunopeptidome Landscape DuringInternational journal of molecular sciences · 2025
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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

10 authors at 4 institutions in 1 country.

Fedra Luciano-MateoDepartment of Medicine and Surgery, Universitat Rovira I Virgili, Reus, Spain.
Noemí CabréDepartment of Medicine and Surgery, Universitat Rovira I Virgili, Reus, Spain.
Salvador Fernández-ArroyoDepartment of Medicine and Surgery, Universitat Rovira I Virgili, Reus, Spain.
Gerard Baiges-GayaUnitat de Recerca Biomèdica, Hospital Universitari Sant Joan, Institut D'Investigació Sanitària Pere Virgili, Reus, Spain.
Anna Hernández-AguileraDepartment of Medicine and Surgery, Universitat Rovira I Virgili, Reus, Spain.
Elisabet Rodríguez-TomàsUnitat de Recerca Biomèdica, Hospital Universitari Sant Joan, Institut D'Investigació Sanitària Pere Virgili, Reus, Spain.
Cristina Muñoz-PinedoCell Death and Metabolism, Institut D'Investigació Biomèdica de Bellvitge, Barcelona, Spain.
Javier A MenéndezProgram Against Cancer Therapeutic Resistance (ProCURE), Metabolism and Cancer Group, Catalan Institute of Oncology, Girona, Spain.
Jordi CampsDepartment of Medicine and Surgery, Universitat Rovira I Virgili, Reus, Spain. jcamps@grupsagessa.com.
Jorge JovenDepartment of Medicine and Surgery, Universitat Rovira I Virgili, Reus, Spain. jjoven@grupsagessa.com.
Institut d'Investigació Sanitària Pere Virgili · ESUniversidad Rovira i Virgili · ESInstitut Català d'Oncologia · ESInstitut d'Investigació Biomédica de Bellvitge · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chemokine (C-C motif) ligand 2 (CCL2) has been associated with chronic metabolic diseases. We aimed to investigate whether Ccl2 gene overexpression is involved in the regulation of signaling pathways in metabolic organs. Biochemical and histological analyses were used to explore tissue damage in cisgenic mice that overexpressed the Ccl2 gene. Metabolites from energy and one-carbon metabolism in liver and muscle extracts were measured by targeted metabolomics. Western blot analysis was used to explore the AMP-activated protein kinase (AMPK) and mammalian target of rapamycin pathways. Ccl2 overexpression resulted in steatosis, decreased AMPK activity and altered mitochondrial dynamics in the liver. These changes were associated with decreased oxidative phosphorylation and alterations in the citric acid cycle and transmethylation. In contrast, AMPK activity and its downstream mediators were increased in muscle, where we observed an increase in oxidative phosphorylation and increased concentrations of different metabolites associated with ATP synthesis. In conclusion, Ccl2 overexpression induces distinct metabolic alterations in the liver and muscle that affect mitochondrial dynamics and the regulation of energy sensors involved in cell homeostasis. These data suggest that CCL2 may be a therapeutic target in metabolic diseases.

Indexed as

Energy MetabolismGene ExpressionAnimalsAutophagyBiopsyChemokine CCL2LiverMaleMetabolic Networks and PathwaysMiceModels, BiologicalMusclesOrgan SpecificityPhenotypeSignal TransductionCCL2 protein, humanChemokine CCL2

Identifiers

PMID32686726
PMCPMC7371894
OpenAlexW3042424058

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Registered trials

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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.