|Title||Cardiac fibroblasts in pressure overload hypertrophy: the enemy within?|
|Publication Type||Journal Article|
|Year of Publication||2014|
|Journal||Journal of Clinical Investigation|
|Pagination||2850 - 2853|
Cardiac fibroblasts have been long recognized as active participants in heart disease; however, their exact physiological and pathological roles remain elusive, mainly due to the lack of specific markers. In this issue of the JCI, Moore-Morris and colleagues used a fibroblast-specific collagen1a1-GFP reporter to demonstrate that fibroblast accumulation after aortic banding in murine hearts arises almost exclusively from proliferation of resident fibroblasts originating from both the epicardium and a previously unrecognized source, the endocardium. Further characterization of fibroblast origin and function in different types and stages of heart disease could lead to development of improved fibroblast-targeted cardiac therapies.
|Short Title||Journal of Clinical Investigation|