Lisa C. Green

This study shows WISP1 drives a unique proliferative and immune-modulatory myofibroblast state in cardiac fibroblasts, acting through a non-canonical P38 MAPK pathway.

This study investigates the molecular mechanisms of HCM caused by the MYBPC3 D389V variant using cardiac organoids and shows hypercontractility and mitochondrial defects that are rescued by a myosin inhibitor.

This study shows that inhibiting HuR reduces cardiac remodeling after ischemia-reperfusion injury by dampening inflammatory gene expression and immune response, but not initial infarct size.

This study shows that HuR-dependent Wisp1 expression is necessary for TGFβ-induced cardiac myofibroblast activity, as HuR inhibition reduces ECM remodeling and contractile functions.