The myofibroblast: one function, multiple origins.

By B. Hinz, S. Phan, V. Thannickal, A. Galli, M. Bochaton-Piallat, G. Gabbiani. American Journal of Pathology, 2007

1,989 citations recorded by the source corpus.

Subfields: Cell Biology, Hepatology, Pulmonary and Respiratory Medicine

View Paper: https://www.semanticscholar.org/paper/599cdad90e7498464f461c3cfa21768a5eedf086

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Citations in the corpus

Pathogenetic mechanisms in radiation fibrosis. (2010, background): “Resident vascular smooth muscle cells (VSMC) are sources of myofibroblasts in atherosclerosis, where they express smooth muscle myosin heavy chain as well as aSMA [25].”
Myofibroblast contraction activates latent TGF-β1 from the extracellular matrix (2007, background): “Furthermore, Mfs drive fi brosis in a variety of other organs that neither exhibit a pronounced epithelium nor posses cells expressing αvβ6 integrin (Hinz et al., 2007).”
The myofibroblast: paradigm for a mechanically active cell. (2010, background): “suitable to rapidly repair injured tissue (Hinz et al., 2007).”
Actin stress fibres (2007, background): “Myofibroblasts in dermal wound tissue arise from the differentiation of tissue fibroblasts (Ross et al., 1970) and circulating fibrocyte progenitors (Hinz et al., 2007), both of which migrate into the centre of the wound site.”
Cancer-Associated Fibroblasts Are Activated in Incipient Neoplasia to Orchestrate Tumor-Promoting Inflammation in an NF-kappaB-Dependent Manner. (2010, background): “Fibroblasts are also key players in wound healing (Hinz et al., 2007; Kisseleva and Brenner, 2008), mediating different aspects of this complex process, including extracellular matrix remodeling and generation of contractile forces.”
The Biological Basis for Cardiac Repair After Myocardial Infarction: From Inflammation to Fibrosis. (2016, background): “Endothelial cells undergoing mesenchymal transdifferentiation,(215) epicardial epithelial cells, and pericytes may represent additional sources of myofibroblasts in the healing infarct.(216) Recent studies using lineage tracing approaches in a model of MI have demonstrated that epicardial-derived ce”
Host Responses in Tissue Repair and Fibrosis (2012, background): “They accumulate in the virtual spaces between organ structures and produce ECM proteins (7), including collagen I and EDA-containing fibronectin (8).”
The myofibroblast matrix: implications for tissue repair and fibrosis (2013, neutral): “A number of recent reviews have considered the nature of myofibroblastprogenitors in different organs [21], including resident fibroblasts [3,19,22-25], fibrocytes[26-28],smooth muscle cells [29], pericytes[30-33], epithelial and endothelial cells undergoing endothelial (EndoMT) or epithelial-to-mes”
Aberrant repair and fibrosis development in skeletal muscle (2011, background): “These cells are associated with tissue repair and fibrosis in many tissues and organs, including muscle, skin, liver, lung, bone and cartilage [56].”
Feedback amplification of fibrosis through matrix stiffening and COX-2 suppression (2010, background): “Regulation of fibroblast matrix synthesis by stiffness Fibroblasts are the major source for excess deposition of extracellular matrix components, including collagen I, in fibrotic disorders (Hinz et al., 2007).”
The IL-1-Like Cytokine IL-33 Is Constitutively Expressed in the Nucleus of Endothelial Cells and Epithelial Cells In Vivo: A Novel ‘Alarmin’? (2008, background): “Specific expression in fibroblasts with myofibroblast characteristics suggests involvement of IL-33 in normal and pathological wound healing, tissue fibrosis and connective-tissue remodeling after injury, processes in which myofibroblasts play critical roles [39,40].”