Schematic diagram illustrating an overview of cellular injury and inflammatory-mediated steps in development of leiomyoma as compared with uterine scar formation caused by mechanical injury (i.e., myomectomy and cesarean delivery)

Schematic diagram illustrating an overview of cellular injury and inflammatory-mediated steps in development of leiomyoma as compared with uterine scar formation caused by mechanical injury (i.e., myomectomy and cesarean delivery). Cellular/tissue injuries and generation of an inflammatory response, either at a small scale (microenvironment) or an extended area (myomectomy/cesarean delivery), results in individual and combined regulatory interactions among several proinflammatory and profibrotic mediators. These mediators, including cytokines, chemokines, growth factors, eicosanoids, proteases, and extracellular matrix (ECM), activate and cause myoblasts and resident fibroblasts differentiation into myofibroblastic phenotype. In addition, possible participation of fibrocytes, which are derived from bone marrow and through circulation reside at the site of inflamed/injury, as well as transformation of vascular endothelial cell into mesenchymal cells, also exist to transform into myofibroblastic phenotype. Collectively, myofibroblasts are highly responsive to the action of various mediators, including cytokines and chemokines, and they produce and deposit various components of ECM that are essential for tissue repair process. Continuous inflammation, excess myofibroblastic transformation, and production of large quantity of ECM with concurrent reduced degradation represent a pathway that leads to development of either leiomyoma and/or scar tissue formation. EGF, endothelial growth factor; FGF, fibroblast growth factor; GM-CSF, granulocyte-macrophage colony-stimulating factor; IGF, insulinlike growth factor; IL, interleukin; LT, leukotriene; MCP, monocyte chemoattractant protein; MIP, macrophage inflammatory protein; MMP, metalloproteinase; PAI, plasminogen activator inhibitor; PG, prostaglandin; RANTES, regulated upon activation, normal T-cell expressed and secreted; TBX, thromboxane; TGF, transforming growth factor; TNF, tumor necrosis factor; TIMP, tissue inhibitor of metalloproteinase; tPA, tissue plasminogen activator; VEGF, vascular endothelial growth factor.

Publication

Proinflammatory and Profibrotic Mediators: Principal Effectors of Leiomyoma Development as a Fibrotic Disorder. () Nasser Chegini. Semin Reprod Med. ;28(3):180-203. Figure: F1. All organisms Homo sapiens Danio rerio

Disease mentions