Abstract
Cardiovascular disease (CVD) is one of the leading causes of death and disability, and has always been a hotspot in clinical and scientific research. The illness brings a heavy economic burden and causes psychological pressure on society and families. The pathogenesis of CVD is complex and has not yet been fully elucidated. Mitochondria provide energy for cardiovascular function. cAMP signaling is closely related to the mechanism of action of mitochondria. Epac, an important effector of cAMP, is involved in a variety of physiopathological mechanisms of CVD. Epac acts on a variety of pathways, including ion level regulation, cardiac hypertrophy, cardiac fibrosis, cardiomyocyte apoptosis, and angiogenesis. In this article, we systematically discuss the mechanism of action of Epac in CVDs to provide (i) ideas for the treatment of CVDs such as arrhythmia and heart failure and (ii) a basis for studying biological pathways and carrying out targeted drug research. Although some of the studied mechanisms are inconsistent, they also illustrate the complexity and importance of the effects of Epac.
NSTL