Evidence map›Paper›PMID 42853539›Full record

ArticleCardiovascular drugs and therapy2026

Epac1 Functions as a Central Cardioprotective cAMP Effector During Ischemic and β-adrenergic Preconditioning.

M S Eriksen, F E Ravn, A Aspevik, J T Haugom, A Wergeland, K S Nordhus, R Kopperud, M Bakke, S O Døskeland, A K Jonassen

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Article in Cardiovascular drugs and therapy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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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

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

M S Eriksen *Faculty for Medicine and Health Science, Institute for Health Science, NTNU, Gjøvik, Norway.
F E Ravn *Department of Biomedicine, Faculty of Medicine, University of Bergen, Bergen, Norway.
A AspevikDepartment of Biomedicine, Faculty of Medicine, University of Bergen, Bergen, Norway.
J T HaugomFaculty for Medicine and Health Science, Institute for Health Science, NTNU, Gjøvik, Norway.
A WergelandDepartment of Biomedicine, Faculty of Medicine, University of Bergen, Bergen, Norway.
K S NordhusDepartment of Biomedicine, Faculty of Medicine, University of Bergen, Bergen, Norway.
R KopperudDepartment of Biomedicine, Faculty of Medicine, University of Bergen, Bergen, Norway.
M BakkeDepartment of Biomedicine, Faculty of Medicine, University of Bergen, Bergen, Norway.
S O DøskelandDepartment of Biomedicine, Faculty of Medicine, University of Bergen, Bergen, Norway.
A K JonassenFaculty for Medicine and Health Science, Institute for Health Science, NTNU, Gjøvik, Norway. anne.jonassen@ntnu.no.ORCID https://orcid.org/0000-0002-6411-4408

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundβ-adrenergic receptor (β-AR) stimulated cAMP signaling may be impaired in pathophysiological conditions such as myocardial ischemia and heart failure, highlighting the need for cardioprotective strategies bypassing β-ARs, directly targeting downstream cAMP effectors. cAMP signaling has traditionally been attributed to protein kinase A (PKA), while contribution of the alternative cAMP effector Epac1 remains controversial.

objectiveTo examine whether Epac1 is required for cardioprotection induced by ischemic preconditioning (IPC) and β-adrenergic preconditioning (β-PC), and to identify downstream signaling pathways.

methodsLangendorff-perfused hearts from wild-type (WT) and Epac1-deficient (Epac1

resultsIPC and β-PC significantly reduced infarct size in WT hearts but failed to confer protection in Epac1

conclusionEpac1 mediates IPC and β-PC induced cardioprotection through Akt/GSK3β- and STAT3-dependent signaling, supporting Epac1 as a promising β-AR-independent therapeutic target.

Indexed as

AktCAMP/PKA/Epac-signalingIschemia–reperfusion injury (IRI)Ischemic/β-adrenergic preconditioning (IPC)Myocardial infarction (MI)STAT3

Identifiers

PMID42853539

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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.