The myofibroblast in wound healing and fibrocontractive diseases

By G. Gabbiani. Journal of Pathology, 2003

1,684 citations recorded by the source corpus.

Subfields: Rehabilitation, Surgery, Urology

View Paper: https://www.semanticscholar.org/paper/b0a698e9caeeac2a18ef90d6c578a165cfa6c4fa

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Citations in the corpus

Macrophages: Master Regulators of Inflammation and Fibrosis (2010, background): “AND ACTIVATE TGF-b1 The TGF-b cytokines (TGF-b1, -b2, and -b3) are induced and activated in a variety of fibrotic diseases, with the TGF-b1 isoform suspected of playing a key role in liver fibrogenesis.31 Early studies of liver fibrosis indicated that damaged hepatocytes and activated HSCs were like”
Myocardial remodeling after infarction: the role of myofibroblasts (2010, background): “Potential differentiation markers Fully differentiated myofibroblasts are characterized by the expression of α-smooth muscle actin (ASMA) and other smooth muscle cell (SMC) differentiation markers ( Figure 2 , Table 1 )”
Macrophages are required for adult salamander limb regeneration (2013, background): “Disruption of collagen production in macrophage-depleted limb stumps is presumably due to the activation of myofibroblasts, which are mainly absent in normal axolotl limb and scar-free skin regeneration (31), contributes to scarring inmammals (50, 51), and represents a major difference between fibro”
Pathophysiology of Myocardial Infarction (2015, neutral): “Additional sources of infarct fibroblasts may include epicardial cells, cardiac pericytes, and vascular smooth muscle cells (128).”
TGF‐β signaling and the fibrotic response (2004, background): “observed in lesions of fibrotic disease (2).”
Formation and function of the myofibroblast during tissue repair. (2007, background): “Moreover, it becomes increasingly clear that myofibroblast development is profoundly influenced by the mechanical microenvironment, in particular, by the organization and stiffness of the ECM (Hinz and Gabbiani, 2003a).”
Myofibroblast contraction activates latent TGF-β1 from the extracellular matrix (2007, positive): “However, the excessive ECM-secreting and contractile activities of Mfs contribute to progressive fi brosis in many organs, such as the heart, lung, liver, kidney, and skin (Gabbiani, 2003; Hinz et al., 2007).”
Integrins and extracellular matrix in mechanotransduction. (2010, background): “, fibroblasts into myofibroblasts) (Gabbiani 2003; Schiller et al. 2004).”
An Essential Role for Senescent Cells in Optimal Wound Healing through Secretion of PDGF-AA. (2026, background): “This contraction is driven mainly by myoﬁbroblasts, which are thought to arise from the conversion of wound site ﬁ-broblasts into a myoﬁbroblastic phenotype (Gabbiani, 2003).”
Cardiac fibroblasts, fibrosis and extracellular matrix remodeling in heart disease (2012, background): “This allows the myoFBs to exert a contractile force on the surrounding ECM [28].”
Wound Healing: A Cellular Perspective. (2019, background): “These cells are formed when fibroblasts acquire bundles of microfilaments in a process regulated by several cellular-ECM interactions, growth factors, and mechanosensory signals within the granulation tissue (130, 162, 353).”
Fibroblasts in fibrosis: novel roles and mediators (2014, background): “Fibroblast to myofibroblast transitioning enables the contraction of the matrix to seal an open wound in the event of the loss of tissue (Gabbiani, 2003; Midwood et al., 2004).”
Fibroblasts in cancer (2006, neutral): “In the absence of electron microscopy validation, CAFs are commonly identified by their expression of α-smooth-muscle acti”