Figure 2.

Schematic representation of cellular transitions contributing to myofibroblasts in endometriotic lesions. Fibroblast-to-myofibroblast transdifferentiation (FMT), epithelial-to-mesenchymal transition (EMT), and, to a lesser extent, endothelial-to-mesenchymal transition (EndoMT) are sources of myofibroblasts in endometriosis, marked by expression of α smooth muscle actin (α-SMA). In FMT, expression of vimentin increases, and fibroblasts thin and elongate. In EMT, the expression of E-cadherin decreases, and expression of vimentin increases. In EndoMT, expression of CD-31 decreases, and expression of fibroblast-specific protein (FSP1) increases. Smooth-muscle-metaplasia (SMM) can lead to smooth muscle-like cells in endometriosis, expressing desmin and smooth muscle myosin heavy chain (SM-MHC).