Aim: Cardiovascular disease (CVD) is the term used to define a group of disorders of the heart and blood vessels. Apoptosis, also known as programmed cell death (PCD), is genetically programmed "cell suicide" that plays an essential role in physiological processes such as embryo development, synaptogenesis, tissue turnover and the negative selection of T-cells, as well as in many diseases, such as cancer, and autoimmune and neurodegenerative diseases. The aim of this paper is to review the most recent data concerning the role of apoptosis in CVD, concentrating on the key apoptotic pathways in cardiomyocytes that may represent potential targets for therapeutic interventions.
Data summary: The function of apoptosis in regulating CVD has recently been extensively investigated as a possible mechanism explaining the pathophysiological significance of various forms of CVD. Despite the difficulties of studying apoptosis in cardiomyocytes, a large number of studies of cellular and animal models suggest that they have the main apoptotic pathways that are also active in other cell types. However, the role of apoptosis in human pathologies, such as heart failure, ischemic heart disease and cardiac hypertrophy is still controversial. We revised classical (TUNEL) and novel experimental approaches (knock-out and transgenic mice; high-throughput genomics and proteomics) to address the role of apoptosis in CVD, concentrating on potential targets for therapeutic intervention.
Conclusion: Knowledge of the basic mechanisms regulating apoptosis activation and inhibition in cardiomyocytes may have important clinical and therapeutic implications.