The Role of EPAC in the Pathogenesis of Cardiovascular Complications: A Review

Cardiovascular disease is a primary cause of mortality and disability and it has long been a focus of clinical and scientific investigation. There is still much to learn about the intricate pathophysiology of cardiovascular disease. The energy needed for circulatory function is provided by mitochondria. Cyclic adenosine monophosphate (cAMP) signalling is directly connected to the mitochondrial action mechanism. cAMP is a ubiquitous second messenger that regulates gene expression, cell shape and function. The identification of the exchange protein directly activated by cAMP (EPAC) eighteen years ago was a significant step towards a better understanding of cAMP signalling. Several studies in the literature have shown that since the introduction of EPAC pharmacological modulators, EPAC plays a critical role in the regulation of many cAMP-determined cardiac functions. The multidomain form of EPAC proteins allows them to be connected to several effectors in different subcellular compartments. Several cardiovascular disorders such as cardiac arrhythmia, atherosclerosis, heart failure, cardiac apoptosis, cardiac hypertrophy and many more, may be treated with these novel cAMP sensors, which are also in connection to several physiological processes. This article provides a discussion of EPAC's mechanism of action in CVDs, which may serve as a platform for targeted pharmacological research and expansion in innovation in the healing of disease processes.