2016
DOI: 10.1007/s40139-016-0099-1
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Fibroblast—Extracellular Matrix Interactions in Tissue Fibrosis

Abstract: Activated myofibroblasts are key effector cells in tissue fibrosis. Emerging evidence suggests that myofibroblasts infiltrating fibrotic tissues originate predominantly from local mesenchyme-derived populations. Alterations in the extracellular matrix network play an important role in modulating fibroblast phenotype and function. In a pro-inflammatory environment, generation of matrix fragments may induce a matrix-degrading fibroblast phenotype. Deposition of ED-A fibronectin plays an important role in myofibr… Show more

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Cited by 42 publications
(32 citation statements)
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References 105 publications
(90 reference statements)
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“…Cardiac repair following myocardial infarction can be divided in three distinct but overlapping phases: the inflammatory phase, the proliferative phase, and the maturation phase [18]. In response to the dramatic changes in the cytokine milieu and to the alterations in composition of the surrounding extracellular matrix following infarction, cardiac fibroblasts exhibit dynamic phenotypic changes during the 3 phases of cardiac repair [5],[19],[20]. …”
Section: Fibroblasts In the Infarcted Myocardiummentioning
confidence: 99%
“…Cardiac repair following myocardial infarction can be divided in three distinct but overlapping phases: the inflammatory phase, the proliferative phase, and the maturation phase [18]. In response to the dramatic changes in the cytokine milieu and to the alterations in composition of the surrounding extracellular matrix following infarction, cardiac fibroblasts exhibit dynamic phenotypic changes during the 3 phases of cardiac repair [5],[19],[20]. …”
Section: Fibroblasts In the Infarcted Myocardiummentioning
confidence: 99%
“…Activated myofibroblasts are key effector cells in all models of fibrosis. In wound healing, tissue strain and cytokine release activate myofibroblasts, which initiate migration, extracellular matrix (ECM) deposition and tissue contraction, thereby maintaining tissue homeostasis (30). However, in fibrosis, an exaggerated myofibroblast response results in inappropriate ECM deposition, increased tissue stiffness and organ dysfunction (31).…”
Section: Discussionmentioning
confidence: 99%
“…In IPF, this remodelling is dysregulated; increased deposition of the individual ECM components partnered with reduced degradation leads to matrix accumulation and fibrosis [117,123]. ECM fragments such as fibrin, fibronectin and hyaluronan are drastically upregulated in fibrotic ECMs, and have profibrotic effects similar to growth factors [124], suggesting that the compositional changes of the fibrotic ECM alone can drive a profibrotic cell phenotype.…”
Section: Ecm Abnormalitymentioning
confidence: 99%