Targeting inflammation to reduce cardiac fibrosis and heart failure

The lack of effective therapies for cardiac fibrosis highlights the urgent need to identify novel therapeutic targets. While anti-fibrosis therapies may have a powerful effect on diastolic dysfunction, such therapies in humans have yielded disappointing results.

We propose a novel approach to this problem by focusing on endothelial inflammation and monocyte-derived macrophage infiltration. Identifying novel anti-inflammatory therapies that reduce cardiac inflammation is a high priority for preventing and treating physiological dysfunction with fibrosis. We investigated the effects of a new drug-free, E-selectin-targeted biomedical polymer on multiple domains of clinically relevant disease. The results of our studies provide initial evidence for both the mechanistic role and therapeutic potential of targeting E-selectin to improve cardiac fibrosis and heart failure.