Mast Cells and Cardiac Fibroblasts
| Autor: | Ryan H. Cunnington, Ian M.C. Dixon |
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| Rok vydání: | 2011 |
| Předmět: | |
| Zdroj: | Hypertension. 58:142-144 |
| ISSN: | 1524-4563 0194-911X |
| Popis: | See related article, pp 264–270 The term “fibroblast” designates a highly heterogenous group of cells that exhibit distinct differentiated phenotypes in different organs.1 The study of fibroblast and myofibroblast biology in specific organs is an important but relatively understudied area, especially in the heart. Recent novel data indicate that ventricular fibroblast activation and cardiac fibrosis are primary events in ventricular remodeling rather than secondary to cardiomyocyte injury.2 In larger mammalian species, including humans, cardiac fibroblasts represent the most numerous nonmyocytes in the myocardium. These cells function to synthesize and organize collagens, fibronectins, and other interstitial components and, thus, maintain the integrity of the cardiac extracellular matrix (matrix). Matrix remodeling can manifest as interstitial fibrosis of an otherwise normal myocardium. This remodeling may occur with the onset of hypertension or as the progressive evolution of the structure of the infarct scar. Remodeling of the matrix occurs later in the noninfarcted myocardium, in the etiology of heart failure after myocardial infarction. The dogma that cardiac fibrosis is merely a secondary disease modifier after cardiomyocyte damage is losing ground to the idea that fibrosis is a primary disease prima facie. Therefore, the need to identify and characterize the specific signals that might trigger the phenoconversion of relatively quiescent fibroblasts to myofibroblasts takes on new importance. In normal heart tissue, matrix protein secretion and deposition are carried out exclusively by cardiac fibroblasts with relatively low turnover of proteins. Conversely, contractile and hypersynthetic myofibroblasts are the relevant phenotypic variants in wound healing or in hypertrophied and … |
| Databáze: | OpenAIRE |
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