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  • Title: Disruption of Epac1 protects the heart from adenylyl cyclase type 5-mediated cardiac dysfunction.
    Author: Cai W, Fujita T, Hidaka Y, Jin H, Suita K, Prajapati R, Liang C, Umemura M, Yokoyama U, Sato M, Okumura S, Ishikawa Y.
    Journal: Biochem Biophys Res Commun; 2016 Jun 17; 475(1):1-7. PubMed ID: 27117748.
    Abstract:
    Type 5 adenylyl cyclase (AC5) plays an important role in the development of chronic catecholamine stress-induced heart failure and arrhythmia in mice. Epac (exchange protein activated by cAMP), which is directly activated by cAMP independent of protein kinase A, has been recently identified as a novel mediator of cAMP signaling in the heart. However, the role of Epac in AC5-mediated cardiac dysfunction and arrhythmias remains poorly understood. We therefore generated AC5 transgenic mice (AC5TG) with selective disruption of the Epac1 gene (AC5TG-Epac1KO), and compared their phenotypes with those of AC5TG after chronic isoproterenol (ISO) infusion. Decreased cardiac function as well as increased susceptibility to pacing-induced atrial fibrillation (AF) in response to ISO were significantly attenuated in AC5TG-Epac1KO mice, compared to AC5TG mice. Increased cardiac apoptosis and cardiac fibrosis were also concomitantly attenuated in AC5TG-Epac1KO mice compared to AC5TG mice. These findings indicate that Epac1 plays an important role in AC5-mediated cardiac dysfunction and AF susceptibility.
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