Evidence map›Paper›PMID 37551870›Full record

ArticleeLife2023

EPAC1 inhibition protects the heart from doxorubicin-induced toxicity.

Marianne Mazevet, Anissa Belhadef, Maxance Ribeiro, Delphine Dayde, Anna Llach, Marion Laudette, Tiphaine Belleville, Philippe Mateo, Mélanie Gressette, Florence Lefebvre and 11 more

Open access · goldAbstract read
In one paragraph

Article in eLife, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.8field-weighted citation impact, top 13% 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

5 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

21 authors at 3 institutions in 2 countries.

Marianne MazevetUniversité Paris-Saclay, Inserm, UMR-S 1180, Orsay, France.
Anissa BelhadefUniversité Paris-Saclay, Inserm, UMR-S 1180, Orsay, France.
Maxance RibeiroUniversité Paris-Saclay, Inserm, UMR-S 1180, Orsay, France.
Delphine DaydeUniversité Paris-Saclay, Inserm, UMR-S 1180, Orsay, France.ORCID https://orcid.org/0000-0001-8543-2352
Anna LlachUniversité Paris-Saclay, Inserm, UMR-S 1180, Orsay, France.
Marion LaudetteInstitut des Maladies Metaboliques et Cardiovasculaires - I2MC, INSERM, Université de Toulouse, Toulouse, France.
Tiphaine BellevilleInnovations Thérapeutiques en Hémostase - UMR-S 1140, INSERM, Faculté de Pharmacie, Université Paris Descartes, Sorbonne Paris Cité, Paris, France.
Philippe MateoUniversité Paris-Saclay, Inserm, UMR-S 1180, Orsay, France.
Mélanie GressetteUniversité Paris-Saclay, Inserm, UMR-S 1180, Orsay, France.
Florence LefebvreUniversité Paris-Saclay, Inserm, UMR-S 1180, Orsay, France.
Ju ChenBasic Cardiac Research UCSD School of Medicine La Jolla, San Diego, United States.
Christilla Bachelot-LozaInnovations Thérapeutiques en Hémostase - UMR-S 1140, INSERM, Faculté de Pharmacie, Université Paris Descartes, Sorbonne Paris Cité, Paris, France.
Catherine Rucker-MartinFaculté de Médecine, Université Paris-Saclay, Le Kremlin Bicêtre, France.
Frank LezoualchInstitut des Maladies Metaboliques et Cardiovasculaires - I2MC, INSERM, Université de Toulouse, Toulouse, France.
Bertrand CrozatierUniversité Paris-Saclay, Inserm, UMR-S 1180, Orsay, France.
Jean-Pierre BenitahUniversité Paris-Saclay, Inserm, UMR-S 1180, Orsay, France.
Marie-Catherine VozeninLaboratoire de Radio-Oncologie, CHUV, Lausanne, Switzerland.ORCID https://orcid.org/0000-0002-2109-8073
Rodolphe FischmeisterUniversité Paris-Saclay, Inserm, UMR-S 1180, Orsay, France.ORCID https://orcid.org/0000-0003-2086-9865
Ana-Maria GomezUniversité Paris-Saclay, Inserm, UMR-S 1180, Orsay, France.
Christophe Lemaire *Université Paris-Saclay, Inserm, UMR-S 1180, Orsay, France.
Eric Morel *Université Paris-Saclay, Inserm, UMR-S 1180, Orsay, France.ORCID https://orcid.org/0000-0003-1960-0121
Inserm · FRDélégation Paris 5 · FRUniversity of California San Diego · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Anthracyclines, such as doxorubicin (Dox), are widely used chemotherapeutic agents for the treatment of solid tumors and hematologic malignancies. However, they frequently induce cardiotoxicity leading to dilated cardiomyopathy and heart failure. This study sought to investigate the role of the exchange protein directly activated by cAMP (EPAC) in Dox-induced cardiotoxicity and the potential cardioprotective effects of EPAC inhibition. We show that Dox induces DNA damage and cardiomyocyte cell death with apoptotic features. Dox also led to an increase in both cAMP concentration and EPAC1 activity. The pharmacological inhibition of EPAC1 (with CE3F4) but not EPAC2 alleviated the whole Dox-induced pattern of alterations. When administered

Indexed as

CardiomyopathiesCardiomyopathy, DilatedAnimalsApoptosisCardiotoxicityDoxorubicinGuanine Nucleotide Exchange FactorsHumansMiceMice, KnockoutMyocytes, CardiacDoxorubicinGuanine Nucleotide Exchange Factorscancer biologycardiologycardiotoxicitycell biologydoxorubicinEPAC1humanmouserat

Identifiers

PMID37551870
PMCPMC10484526
OpenAlexW4385660764

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.