6 November 2014 | Ian A Darby, Betty Laverder, Frédéric Bonté, Alexis Desmoulière
The article "Fibroblasts and Myofibroblasts in Wound Healing" by Ian A. Darby, Betty Laverdet, Frédéric Bonté, and Alexis Desmoulère, published in *Clinical, Cosmetic and Investigational Dermatology*, discusses the role of (myo)fibroblasts in maintaining skin homeostasis and orchestrating tissue repair. (Myo)fibroblasts are embedded in a complex extracellular matrix (ECM) and interact with their microenvironment through secretion of ECM components, matrix metalloproteinases, and tissue inhibitors of metalloproteinases. They play a crucial role in cell differentiation, proliferation, quiescence, and apoptosis, as well as in regulating growth factor bioavailability. The phenotype of (myo)fibroblasts is influenced by mechanical stresses, which can lead to pathological conditions such as excessive scarring or fibrosis. The article also explores the origin of wound myofibroblasts, including local connective tissue fibroblasts, mesenchymal stem cells, fibrocytes, and cells derived from epithelial-to-mesenchymal transition processes. Additionally, it examines the role of mechanical forces, hypoxia, and therapies in regulating myofibroblast activity. The authors highlight the importance of understanding the interactions between (myo)fibroblasts and their microenvironment to develop new therapeutic approaches for preventing or treating pathological conditions.The article "Fibroblasts and Myofibroblasts in Wound Healing" by Ian A. Darby, Betty Laverdet, Frédéric Bonté, and Alexis Desmoulère, published in *Clinical, Cosmetic and Investigational Dermatology*, discusses the role of (myo)fibroblasts in maintaining skin homeostasis and orchestrating tissue repair. (Myo)fibroblasts are embedded in a complex extracellular matrix (ECM) and interact with their microenvironment through secretion of ECM components, matrix metalloproteinases, and tissue inhibitors of metalloproteinases. They play a crucial role in cell differentiation, proliferation, quiescence, and apoptosis, as well as in regulating growth factor bioavailability. The phenotype of (myo)fibroblasts is influenced by mechanical stresses, which can lead to pathological conditions such as excessive scarring or fibrosis. The article also explores the origin of wound myofibroblasts, including local connective tissue fibroblasts, mesenchymal stem cells, fibrocytes, and cells derived from epithelial-to-mesenchymal transition processes. Additionally, it examines the role of mechanical forces, hypoxia, and therapies in regulating myofibroblast activity. The authors highlight the importance of understanding the interactions between (myo)fibroblasts and their microenvironment to develop new therapeutic approaches for preventing or treating pathological conditions.