The Origin of Fibroblasts and Mechanism of Cardiac Fibrosis

By G. Krenning, E. Zeisberg, Raghu Kalluri. Journal of Cellular Physiology, 2010

626 citations recorded by the source corpus.

Fibroblasts are at the heart of cardiac function and are the principal determinants of cardiac fibrosis. Nevertheless, cardiac fibroblasts remain poorly characterized in molecular terms. Evidence is evolving that the cardiac fibroblast is a highly heterogenic cell population, and that such heterogeneity is caused by the distinct origins of fibroblasts in the heart. Cardiac fibroblasts can derive either from resident fibroblasts, from endothelial cells via an endothelial–mesenchynmal transition or from bone marrow‐derived circulating progenitor cells, monocytes and fibrocytes. Here, we review the function and origin of fibroblasts in cardiac fibrosis.NB. The information given is correct. J. Cell. Physiol. 225: 631–637, 2010. © 2010 Wiley‐Liss, Inc.

Subfields: Cancer Research, Cardiology and Cardiovascular Medicine, Surgery

View Paper: https://www.semanticscholar.org/paper/f95d10dfb4416a898191bb0b7cf7c0115742d2d3

How researchers see this paper

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In Cancer Research

1. H. Ruskoaho
2. Virpi Talman
3. A. Takawale
4. Z. Kassiri
5. Nikolaos G. Frangogiannis

In Cardiology and Cardiovascular Medicine

1. Nikolaos G. Frangogiannis
2. H. Ruskoaho
3. Virpi Talman
4. A. Takawale
5. Z. Kassiri

In Surgery

1. Nikolaos G. Frangogiannis
2. H. Ruskoaho
3. Virpi Talman

Citations in the corpus

• Cardiac fibroblasts, fibrosis and extracellular matrix remodeling in heart disease (2012, background): “Perivascular cells, such as pericytes, have been shown to differentiate into collagen-producing FBs in the kidney [51] and in the retina in vitro [52], but the contribution of these cells in formation of CFBs has not yet been determined [6].”
• Cardiac fibrosis in myocardial infarction—from repair and remodeling to regeneration (2016, background): “According to earlier studies, fibroblasts were considered the most abundant nonmyocyte cell type, even outnumbering cardiomyocytes in adult mammalian hearts (Banerjee et al. 2007; Krenning et al. 2010; Zeisberg and Kalluri 2010; Deb and Ubil 2014).”
• The myofibroblast matrix: implications for tissue repair and fibrosis (2013, neutral): “The contribution of myofibroblastsand their elaborated ECM to normal and pathologic tissue repair [3]has been well-studied in lung [4-6], liver [7-9], kidney [10,11], skeletal muscle [12], systemic sclerosis [13-15], heart [16-18], and the stromal reaction to tumours[19,20].”
• TGF-β signaling in fibrosis (2011, background): “In addition to mesenchymal cells, myofibroblasts may derive from epithelial origin in a process termed epithelial–mesenchymal transition (EMT) (Krenning et al. 2010).”