Evidence map›Paper›PMID 39885113›Full record

ArticleGeroScience2025

Comparative phenotyping of C57BL/6J substrains reveals distinctive patterns of cardiac aging.

Sophia Walter, Patricia Baumgarten, Niklas Hegemann, Steffen P Häseli, Stefanie Deubel, Julia Jelleschitz, Annika Höhn, Nikolaus Berndt, Wolfgang M Kuebler, Jana Grune and 1 more

Abstract readComparative Study
In one paragraph

Article in GeroScience, 2025. 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
–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

4 citing papers in PubMed.

  1. From bump to pump: extracellular matrix remodeling, dynamics, and biomechanics in the maternal heart.American journal of physiology. Heart and circulatory physiology · 2026
    Review
  2. Article
  3. Article
  4. 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

11 authors.

Sophia WalterMolecular Toxicology, German Institute of Human Nutrition Potsdam-Rehbruecke (DIfE), Nuthetal, Germany.
Patricia BaumgartenMolecular Toxicology, German Institute of Human Nutrition Potsdam-Rehbruecke (DIfE), Nuthetal, Germany.
Niklas HegemannDZHK (German Center for Cardiovascular Research), Partner Site Berlin, Berlin, Germany.
Steffen P HäseliMolecular Toxicology, German Institute of Human Nutrition Potsdam-Rehbruecke (DIfE), Nuthetal, Germany.
Stefanie DeubelMolecular Toxicology, German Institute of Human Nutrition Potsdam-Rehbruecke (DIfE), Nuthetal, Germany.
Julia JelleschitzMolecular Toxicology, German Institute of Human Nutrition Potsdam-Rehbruecke (DIfE), Nuthetal, Germany.
Annika HöhnMolecular Toxicology, German Institute of Human Nutrition Potsdam-Rehbruecke (DIfE), Nuthetal, Germany.
Nikolaus BerndtMolecular Toxicology, German Institute of Human Nutrition Potsdam-Rehbruecke (DIfE), Nuthetal, Germany.
Wolfgang M KueblerInstitute of Physiology, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität Zu Berlin, Charitéplatz 1, 10117, Berlin, Germany.
Jana GruneDZHK (German Center for Cardiovascular Research), Partner Site Berlin, Berlin, Germany.
Christiane OttMolecular Toxicology, German Institute of Human Nutrition Potsdam-Rehbruecke (DIfE), Nuthetal, Germany. Christiane.ott@dife.de.ORCID 0000-0002-3199-0655

Funding

Deutsche Forschungsgemeinschaft 491394008Deutsche Forschungsgemeinschaft FOR 2558Deutsche Forschungsgemeinschaft Gr1240/25-1Deutsche Forschungsgemeinschaft SFB-1470- A04Deutsche Forschungsgemeinschaft SFB-1470- A08Deutsches Zentrum für Diabetesforschung 82DZD03D03Deutsches Zentrum für Herz-Kreislaufforschung 81Z2100502
6 · The paper itself

Abstract

Research in aging often refers to animal models, particularly C57BL/6J (B6J) mice, considered gold standard. However, B6J mice are distributed by different suppliers, which results in divers substrains exhibiting notable phenotypic differences. To ensure a suitable phenotype of cardiac aging, we performed heart analyses of young (5 months) and old B6J mice (24 months) from two substrains: B6JRj (Janvier) and B6JCrl mice (Charles River). In hearts of both substrains, myocardial fibrosis increased with age; however, only in old B6JRj mice cardiac hypertrophy associated with a decreased ejection fraction was observed. Gene set enrichment analysis in heart tissue using proteomic data revealed different age-associated pathway changes between the substrains, especially in oxidative phosphorylation. Functional assessment of isolated cardiomyocytes verified cardiac impairment during aging in B6JRj mice. Overall, results demonstrate that cardiac aging manifests as a moderate systolic dysfunction in B6JRj mice, while B6JCrl mice display no functional changes with age.

Indexed as

AgingHeartMyocardiumAnimalsCardiomegalyMaleMiceMice, Inbred C57BLMyocytes, CardiacPhenotypeCardiac aging phenotypeCardiomyocyteEchocardiographyHeart failureProteomics

Identifiers

PMID39885113
PMCPMC12181499

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.