| pubmed-article:20635395 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:20635395 | lifeskim:mentions | umls-concept:C0018787 | lld:lifeskim |
| pubmed-article:20635395 | lifeskim:mentions | umls-concept:C0016030 | lld:lifeskim |
| pubmed-article:20635395 | lifeskim:mentions | umls-concept:C0016059 | lld:lifeskim |
| pubmed-article:20635395 | lifeskim:mentions | umls-concept:C0439659 | lld:lifeskim |
| pubmed-article:20635395 | lifeskim:mentions | umls-concept:C0441712 | lld:lifeskim |
| pubmed-article:20635395 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:20635395 | pubmed:dateCreated | 2010-9-15 | lld:pubmed |
| pubmed-article:20635395 | pubmed:abstractText | 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. | lld:pubmed |
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