Journal
JOURNAL OF MOLECULAR MEDICINE-JMM
Volume 93, Issue 8, Pages 823-830Publisher
SPRINGER
DOI: 10.1007/s00109-015-1314-y
Keywords
Cardiac fibroblast; Hypertrophy; Fibrosis
Funding
- WHRI-COFUND
- Leducq Foundation
- Lefoulon-Delalande foundation
- NIH/NHLBI [P01HL069779]
- National Heart, Lung, and Blood Institute
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Cardiac fibroblasts are a major cell population of the heart and are characterized by their capacity to produce extracellular matrix (ECM). In hearts subjected to pressure overload, excessive fibroblast accumulation is responsible for fibrosis of the myocardium, a major clinical issue. Hence, understanding mechanisms generating fibroblasts in this context has become a key question in the cardiovascular field. Recent studies now point to the activation of resident fibroblasts as the underlying cause of fibrosis. However, de novo generation of fibroblasts from endothelium and circulating hematopoietic cells has also been proposed to significantly contribute to fibrosis. Here, we discuss the latest findings on fibroblast origins, with a particular emphasis on the pressure overload model, and the implication of these findings for the development of anti-fibrotic therapies that are currently lacking.
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