Evidence map›Paper›PMID 23741376›Full record

ArticlePloS one2013

Increased beta2-adrenoceptors in doxorubicin-induced cardiomyopathy in rat.

Nolwenn Merlet, Nicolas Piriou, Bertrand Rozec, Amandine Grabherr, Benjamin Lauzier, Jean-Noël Trochu, Chantal Gauthier

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.0field-weighted citation impact, top 21% 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

23 citing papers in PubMed, 42 citations in OpenAlex.

  1. Review
  2. Article
  3. Drug Repositioning in Doxorubicin-Induced Cardiotoxicity Protection.International journal of molecular sciences · 2025
    Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
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  12. AnInternational journal of molecular sciences · 2021
    Article
  13. Article
  14. Implications of a Soy-Based Diet for Animal Models.International journal of molecular sciences · 2021
    Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Carvedilol Prevents Redox Inactivation of Cardiomyocyte ΒJACC. Basic to translational science · 2018
    Article
  20. 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

7 authors at 4 institutions in 1 country.

Nolwenn Merletl'institut du thorax, Unité Inserm UMR 1087/CNRS UMR 6291, Nantes, France.
Nicolas Piriou
Bertrand Rozec
Amandine Grabherr
Benjamin Lauzier
Jean-Noël Trochu
Chantal Gauthier
Institut du Thorax · FRInserm · FRCentre Hospitalier Universitaire de Nantes · FRNantes Université · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe toxicity of doxorubicin, leading to an irreversible heart failure, limits its use as chemotherapeutic agent. The beneficial effects of early administration of β-blocker were reported in patients with heart failure due to doxorubicin, suggesting an important role of β-adrenoceptors (β-ARs). This study aimed to identify a putative target (β-AR and/or its effectors) at the early phase of a chronic doxorubicin-induced cardiomyopathy (Dox-CM) in a rat model. METHODOLOGY: Dox-CM was induced by six doxorubicin injections (cumulative dose: 15 mg x kg(-1)) and validated by echocardiography and left ventricle (LV) catheterization. The β-AR protein expressions in LV were evaluated by western-blot at days 35 (d35) and 70 (d70) after the first doxorubicin injection. Ex vivo cardiac contractility (dP/dtmax, dP/dtmin) was evaluated on isolated heart in response to specific β-AR stimulations at d35.

resultsAt d35, Dox-CM hearts were characterized by mild LV systolic and diastolic dysfunctions, which were exacerbated at d70. In Dox-CM hearts, β3-AR expression was only decreased at d70 (-37±8%). At d35, β1-AR expression was decreased by 68±6%, but ex vivo β1-AR function was preserved due to, at least in part, an increased adenylyl cyclase response assessed by forskolin. β2-AR expression was increased both at d35 (+58±22%) and d70 (+174±35%), with an increase of ex vivo β2-AR response at d35. Inhibition of Gi protein with pertussis toxin did not affect β2-AR response in Dox-CM hearts, suggesting a decoupling of β2-AR to Gi protein.

conclusionThis study highlights the β1/β2-AR imbalance in early Dox-CM and reveals the important role that β2-AR/Gi coupling could play in this pathology. Our results suggest that β2-AR could be an interesting target at early stage of Dox-CM.

Indexed as

Adrenergic beta-AntagonistsAnimalsCardiomyopathiesCardiotonic AgentsColforsinDoxorubicinGene Expression RegulationGTP-Binding Protein alpha Subunits, Gi-GoHeartIsoproterenolMaleMyocardial ContractionPertussis ToxinRatsRats, Sprague-DawleyReceptors, Adrenergic, beta-1Adrenergic beta-AntagonistsCardiotonic AgentsColforsinDoxorubicinGTP-Binding Protein alpha Subunits, Gi-GoIsoproterenolPertussis ToxinReceptors, Adrenergic, beta-1Receptors, Adrenergic, beta-2Receptors, Adrenergic, beta-3

Identifiers

PMID23741376
PMCPMC3669386
OpenAlexW2042008955

What Socratic 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 Socratic graph.