Journal
CIRCULATION RESEARCH
Volume 116, Issue 7, Pages 1269-1276Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/CIRCRESAHA.116.305381
Keywords
cicatrix; endothelins; fibrosis; platelet-derived growth factor
Funding
- Canadian Institute of Health Research
- Scleroderma Society of Ontario
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Fibrotic diseases are a significant global burden for which there are limited treatment options. The effector cells of fibrosis are activated fibroblasts called myofibroblasts, a highly contractile cell type characterized by the appearance of alpha-smooth muscle actin stress fibers. The underlying mechanism behind myofibroblast differentiation and persistence has been under much investigation and is known to involve a complex signaling network involving transforming growth factor-beta, endothelin-1, angiotensin II, CCN2 ( connective tissue growth factor), and platelet-derived growth factor. This review addresses the contribution of these signaling molecules to cardiac fibrosis.
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