Sasha Smolgovsky

Recently, the Alcaide lab has begun investigating mechanisms of T cell-mediated cardiac pathology in heart failure with preserved ejection fraction (HFpEF), a condition which comprises half of HF diagnoses, has few direct treatment options, rising incidence, and no cure. A key characteristic of HFpEF is systemic chronic low-grade inflammation, which is also independently associated with HFpEF comorbidities such as obesity and hypertension. While obesity and hypertension each induce specific T cell immune responses, they do not independently induce HFpEF, and whether their combination induces specific T cell immune responses that contribute to HFpEF remains unknown. Using a recently established mouse model of HFpEF induced by obesity and hypertension in combination, we are studying how cell-intrinsic stress resulting from combined comorbidities reprograms T cell activity towards a cardiac inflammatory potential, resulting in specific contributions to cardiac remodeling in HFpEF.