title: Cardiac fibroblasts in pressure overload hypertrophy: the enemy within?
abstract: 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.
authors.forename: Nenad
authors.initials: N
authors.lastname: Bursac
mesh_terms: D000818:Animals; D006333:Heart Failure / Q000473:pathology*; D008297:Male; D009206:Myocardium / Q000473:pathology*