[Cellular and molecular mechanisms of fibrosis].

By J. Scoazec, F. Verrecchia, M. Jacob, P. Bruneval. Annales de Pathologie, 2006

2,133 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/81340f5552ce64da13160b5ed2468970e9204bd0

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

1. TA Wynn
2. Jeremy S. Duffield
3. S. Friedman
4. P. Murray
5. B. Brown
6. D. Sheppard
7. Luke Barron
8. M. Wilson

Citations in the corpus

• Feedback amplification of fibrosis through matrix stiffening and COX-2 suppression (2010, background): “Much attention has focused on the role that soluble inflammatory and fibrogenic mediators play in the initiation and progression of fibrosis (Wynn, 2008).”
• Aberrant repair and fibrosis development in skeletal muscle (2011, background): “As described above, M2a macrophages have been shown to promote fibrosis in several different pathogenic conditions [12], thus supporting the notion that fibrin(ogen) may promote fibrosis by sustaining alternatively activated macrophages in dystrophic muscle.”
• Wound repair at a glance (2009, background): “which can contribute to numerous pathologies (Coussens and Werb, 2002; Wynn, 2008).”
• Bleomycin and IL-1β–mediated pulmonary fibrosis is IL-17A dependent (2010, background): “The possible connection between IL17A expression and Th2 dependent fibrosis, however, has not been previously inves tigated (Wynn, 2008).”
• The Matricellular Protein CCN1/CYR61 Induces Fibroblast Senescence and Restricts Fibrosis in Cutaneous Wound Healing (2010, background): “CCN1-regulated senescence restricts fibrosis in cutaneous wound healing The fibrogenic response contributes to tissue repair by helping to reconstitute the damaged tissue through ECM deposition, although excessive fibrosis may impair tissue functio”
• Myocardial remodeling after infarction: the role of myofibroblasts (2010, background): “Myofibroblasts are thought to be derived from multiple sources ( Figure 1 )”
• Macrophage polarization: An opportunity for improved outcomes in biomaterials and regenerative medicine (2012, background): “Persistent or dysregulated inflammation can result in fibrosis following tissue injury or in the setting of infection [101,102].”
• Protective and pathogenic functions of macrophage subsets (2011, background): “Indeed, they produce matrix metalloproteinases (MMPs) and TIMPs that control ECM turnove”
• Host Responses in Tissue Repair and Fibrosis (2012, background): “These cells, in turn, secrete various wound-healing/profibrotic cytokines, including platelet-derived growth factor (PDGF), transforming growth factor (TGF)-β1, and interleukin (IL)-13 (3).”
• Epithelial to Mesenchymal Transition induces cell cycle arrest and parenchymal damage in renal fibrosis (2015, unknown): “Inflammation has been widely described to be a key driver of kidney fibrosis 42 .”
• The myofibroblast matrix: implications for tissue repair and fibrosis (2013, unknown): “Myofibroblasts are the primary extracellular matrix (ECM)-secreting cells during wound healing and fibrosis, and are largely responsible for the contractility of scar tissue as it matures [1,2].”
• Mechanisms of mesenchymal stem/stromal cell function (2016, background): “Current clinical strategies generally have poor outcomes in terms of efficacy and adverse effects [106].”
• Macrophages in skin injury and repair. (2011, unknown): “Additionally, they promote a Th2 response, which has been linked to fibrinogenesis (Wynn 2008).”