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Published on: June 14, 2016
Cardiac fibroblasts: from development to heart failure
Thomas Moore-Morris1, Nuno Guimarães-Camboa, Katherine E Yutzey
1INSERM UMR_S910, GMGF, University Aix-Marseille, Marseille, France.
Insights
Cardiac fibroblast activation drives myocardial fibrosis during pressure overload. New research explores fibroblast origins, including resident cell activation and de novo generation, to inform anti-fibrotic therapies.
Area of Science:
- Cardiovascular Biology
- Fibrosis Research
- Cellular Origins
Background:
- Cardiac fibroblasts are key extracellular matrix (ECM) producers in the heart.
- Myocardial fibrosis, due to excessive fibroblast accumulation, is a major clinical issue in pressure overload conditions.
- Understanding fibroblast generation mechanisms is crucial for developing effective anti-fibrotic therapies.
Purpose of the Study:
- To review recent findings on the origins of cardiac fibroblasts.
- To emphasize the role of fibroblast origins in the context of pressure overload.
- To discuss the implications for developing novel anti-fibrotic treatments.
Main Methods:
- Review of current scientific literature.
- Focus on studies investigating fibroblast origins in pressure overload models.
- Analysis of proposed mechanisms for fibroblast generation.
Main Results:
- Recent evidence suggests activation of resident cardiac fibroblasts is a primary driver of fibrosis.
- De novo generation of fibroblasts from endothelial and circulating hematopoietic cells also significantly contributes to fibrosis.
- Multiple cellular origins contribute to the fibroblast pool during cardiac pressure overload.
Conclusions:
- Fibrosis in pressure overload is driven by both resident fibroblast activation and de novo fibroblast generation.
- Elucidating these diverse origins is critical for advancing anti-fibrotic therapeutic strategies.
- Targeting specific fibroblast origins may offer new avenues for treating myocardial fibrosis.
Abstract:
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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