Targeting T-cell infiltration and its downstream effects on fibrosis and hypertrophy may represent a novel translational therapeutic approach for nonischemic heart failure.
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May identify T-cell infiltration as a therapeutic target in nonischemic HF; hypothesis-generating and requires human validation.
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.
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Nevers et al. (2015) studied this question.
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