Molecular and Cellular Mechanisms of Heart Disease

Dear Colleagues,

Heart failure is still a leading cause of mortality worldwide. Cardiomyocytes contribute to heart failure by losing the ability to generate sufficient force to pump blood into circulation. To improve the current treatment options in cardiology, it is important to have a better understanding of the biological behavior of cardiomyocytes. The function of these cells cannot be completely understood independently of the interaction with surrounding cells, i.e., cardiac fibroblasts and vascular cells. Nevertheless, cardiomyocytes are the cells that must generate heart work. They can modify parts of their electromechanical coupling machinery, electrometabolic coupling, or increase in size via hypertrophy. However, hypertrophy can be either adaptive or maladaptive, and the transition from the one into the other type of hypertrophy is not clearly understood. Pathological hypertrophy is often characterised by cardiac fibrosis and contributes to cardiac dysfunction. Cell death, i.e., cardiomyocyte apoptosis, is another common feature of heart disease. Processes dealing with metabolism and mitochondrial function, electromechanical coupling, cell death, and electrophysiological aspects are among the processes that need to be addressed and understood in their molecular fine regulation in order to improve treatment regimes.

This Topic aims to summarize the current understanding of the process of developing heart failure with a focus on the force-generating cell, the cardiomyocyte.

Prof. Dr. Pasi Tavi
Prof. Dr. Ebru Arioglu-Inan
Topic Editors