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Myofibroblasts upregulate the expression of fibronectin, collagens, and hyaluronic acid during and after their differentiation from fibroblasts. Among these, the EDA isoform of fibronectin (EDA-FN), and collagen type I (COL1A1/COL1A2) are typical markers of myofibroblast-dependent synthesis of pro-fibrotic extracellular matrix.
Airway remodelling is a multifaceted process involving multiple airway tissues. These include goblet cell hyperplasia, leading to increased mucus production, and airway smooth muscle hypertrophy (or smooth muscle cell hyperplasia), leading to the release of pro-inflammatory and pro-fibrotic messengers contributing to subepithelial fibrosis.
A fibroblast is a type of biological cell typically with a spindle shape [1] that synthesizes the extracellular matrix and collagen, [2] produces the structural framework for animal tissues, and plays a critical role in wound healing. [3]
The normal fibroblast cells receive a hormone signal from nearby cancer cells, indicating that it must become activated, and is thus classed as a CAF. [2] It is unclear why normal fibroblasts transition into CAFs but it has been found that by adding transforming growth factor-β to fibroblasts in culture they start to display features of CAFs. [26]
Histopathologically, FMTs consist of neoplastic connective tissue cells which have differented into cells that have microscopic appearances resembling fibroblasts and/or myofibroblasts. The fibroblastic cells are characterized as spindle-shaped cells with inconspicuous nucleoli that express vimentin , an intracellular protein typically found in ...
This process induces the fibroblast to take up a myofibroblast phenotype and contributes to cancer invasion. FHL2 can also induce EMT and cancer cell migration by affecting the structural integrity of membrane-associated E-cadherin-β-catenin complex. [43]
EGFR has been shown to play a critical role in TGF-beta1 dependent fibroblast to myofibroblast differentiation. [26] [27] Aberrant persistence of myofibroblasts within tissues can lead to progressive tissue fibrosis, impairing tissue or organ function (e.g. skin hypertrophic or keloid scars, liver cirrhosis, myocardial fibrosis, chronic kidney ...
Timing is important to wound healing. Critically, the timing of wound re-epithelialization can decide the outcome of the healing. [11] If the epithelization of tissue over a denuded area is slow, a scar will form over many weeks, or months; [12] [13] If the epithelization of a wounded area is fast, the healing will result in regeneration.