4.7 Review

Getting to the Heart of the Matter New Insights Into Cardiac Fibrosis

Journal

CIRCULATION RESEARCH
Volume 116, Issue 7, Pages 1269-1276

Publisher

LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/CIRCRESAHA.116.305381

Keywords

cicatrix; endothelins; fibrosis; platelet-derived growth factor

Funding

  1. Canadian Institute of Health Research
  2. 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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