Formation and Function of the Myofibroblast during Tissue Repair
2007; Elsevier BV; Volume: 127; Issue: 3 Linguagem: Inglês
10.1038/sj.jid.5700613
ISSN1523-1747
Autores Tópico(s)Tendon Structure and Treatment
ResumoIt is generally accepted that fibroblast-to-myofibroblast differentiation represents a key event during wound healing and tissue repair. The high contractile force generated by myofibroblasts is beneficial for physiological tissue remodeling but detrimental for tissue function when it becomes excessive such as in hypertrophic scars, in virtually all fibrotic diseases and during stroma reaction to tumors. Specific molecular features as well as factors that control myofibroblast differentiation are potential targets to counteract its development, function, and survival. Such targets include α-smooth muscle actin and more recently discovered markers of the myofibroblast cytoskeleton, membrane surface proteins, and the extracellular matrix. Moreover, intervening with myofibroblast stress perception and transmission offers novel strategies to reduce tissue contracture; stress release leads to the instant loss of contraction and promotes apoptosis. It is generally accepted that fibroblast-to-myofibroblast differentiation represents a key event during wound healing and tissue repair. The high contractile force generated by myofibroblasts is beneficial for physiological tissue remodeling but detrimental for tissue function when it becomes excessive such as in hypertrophic scars, in virtually all fibrotic diseases and during stroma reaction to tumors. Specific molecular features as well as factors that control myofibroblast differentiation are potential targets to counteract its development, function, and survival. Such targets include α-smooth muscle actin and more recently discovered markers of the myofibroblast cytoskeleton, membrane surface proteins, and the extracellular matrix. Moreover, intervening with myofibroblast stress perception and transmission offers novel strategies to reduce tissue contracture; stress release leads to the instant loss of contraction and promotes apoptosis. α-smooth muscle actin extracellular matrix focal adhesion found in inflammatory zone fibronectin latency-associated protein latent TGFβ1-binding protein smooth muscle cell transforming growth factor
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