A gradual loss and impaired function of capillaries during the course of life drive overall organismal aging and dysfunction across multiple organs. Within a hypertrophic heart, limited microvascular growth also accelerates the decline in cardiac function, ultimately leading to the onset of heart failure – a prevalent cause of morbidity and mortality in our aging societies. In this project, we will investigate the signals and mechanisms governing age-dependent interactions between cardiomyocytes and their surrounding microvascular environment with the aim to develop novel therapies for the prevention or treatment of heart failure and potentially other age-related cardiac disorders.
