As protein kinase G activity diminishes, cardiomyocytes undergo hypertrophic changes. Endothelial cells also are responsible for the production of E-selectin, which recruits lymphocytes into the tissue beneath the endothelium that subsequently release transforming growth factor beta, encouraging fibrosis and thus ventricular stiffening. Cardiac macrophages are thought to play an important roll in the development of fibrosis as they are increased in HFpEF and release pro-fibrotic cytokines, such as IL-10.[9] [10] Further investigation of the role of inflammation in HFpEF is needed.