Targeting T-cell infiltration and its downstream effects on fibrosis and hypertrophy may represent a novel translational therapeutic approach for nonischemic heart failure.
T cells are major contributors to nonischemic HF. Their activation combined with the activation of the LV endothelium results in LV T-cell infiltration negatively contributing to HF progression through mechanisms involving cytokine release and induction of cardiac fibrosis and hypertrophy. Reduction of T-cell infiltration is thus identified as a novel translational target in HF.
Nevers et al. (Fri,) studied this question.