Cells once viewed as menders may harm the heart

Fibroblasts, cells that repair heart damage, might cause a cycle of stiffening and scarring in certain heart conditions. Dilated cardiomyopathy, a leading cause of heart failure, has been seen as rooted in defective heart muscle cells. But the heart is a complex system of interacting cell types.  

A study published Sept. 11 in Science reexamined the role of fibroblasts and found they might be contributing to the disorder. Drs. Kristi Kooiker, research scientist, and Farid Moussavi-Harami, associate professor (Cardiology) from the Department of Medicine are co-authors.

“Most heart conditions have a fibrotic response that can be harmful,” said Moussavi-Harami. “But we don’t have many therapies to address it. The uniqueness of this study is that we show functional improvement by knocking out the p38 pathway that drives fibrosis. I think that this strategy, in combination with other therapies like myosin activators, could be beneficial for patients who have genetic cardiomyopathies like DCM.”  

Moussavi-Harami imagines that patients might someday be classified by fibrosis level —high, medium or low — to guide personalized treatments.