Heart failure is the most costly medical condition among the elderly in Japan, and although there are various therapeutic agents available, the 5-year survival rate is not high and still claims the lives of many patients.
We have shown that cardiac macrophages interact with cardiomyocytes and are essential for cardiac homeostasis, and that elimination or genetic modification of macrophages to induce loss of function results in death from heart failure and fatal arrhythmias.
The most potent risk factor for heart failure is aging. The mechanism of age-related deterioration of cardiac function is currently unknown, and, of course, there is no treatment for it. In this study, we will examine how cardiac macrophages and other immune cells in the heart change with age and how they adversely affect the heart. We will examine not only the relationship between macrophages and cardiac myocytes, but also their interaction with cardiac fibroblasts and blood vessels.
In addition, the extent to which aging immune system cells within the heart are involved in cardiac aging will be examined to identify novel therapeutic targets in age-related heart failure.