Thomas Vigil

Richard Mortensen Lab


Hypertensive heart disease is a risk factor for morbidity and mortality and is associated with high blood pressure and hypertensive cardiac remodeling.  Common characteristics seen in hypertensive disease include cardiac fibrosis and left ventricular (LV) hypertrophy, both of which are detrimental responses to cardiac injury that can lead to dysfunction and congestive heart failure.  It has been established that proinflammatory immune cell infiltration is a driving force behind hypertensive cardiac remodeling and this can occur in an angiotensin II (Ang II) dependent manner.  The molecular mechanism driving this cardiac inflammatory response and cardiac remodeling remains unclear.  It is well established that infiltration of inflammatory cells including T cells, mast cells, neutrophils, and macrophages are involved in the development of hypertensive cardiac remodeling. There is a growing field of evidence supporting a connection between fibrosis development and macrophages due to their ability to produce profibrotic mediators such as TGF-β that lead to fibroblast activation.  Hypertensive cardiac remodeling is marked with changes in cardiac tissue composition including fibrosis development and left ventricular hypertrophy. A recent study has shown Serum-glucocorticoid regulated kinase 1 (SGK1) may impact macrophage polarization and infiltration in a model of hypertension induced cardiac injury.  My research focus will be to identify the role of SGK1 in myeloid cells during hypertensive cardiac remodeling, specifically focusing on macrophage polarization.