ArticleCardiovascular drugs and therapy2026
Epac1 Functions as a Central Cardioprotective cAMP Effector During Ischemic and β-adrenergic Preconditioning.
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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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.
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