Abstract
Of the myriad of growth factors examined for their ability to accelerate or improve tissue repair, none has as broad a spectrum of action as that of TGF-beta. In the 10 years since the first description of its ability to enhance wound healing, tremendous advances have been made in understanding the basis of its action in tissue repair. It is released from activated platelets and can both act on and be secreted by each of the diverse cell types which participate in the healing process. Actions of TGF-beta to stimulate chemotaxis, fibrogenesis, angiogenesis, and autoinduction of its expression are mediated by signalling through a unique set of serine-threonine kinase receptors which distinguish it mechanistically from other growth factors with activities in wound healing. Both topical and systemic administration of TGF-beta have been shown to improve healing in a variety of animal models of both normal and impaired healing at dermal as well as nondermal sites such as bone, intestine, the eye, or the mouth.
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