Roberts A B
Laboratory of Chemoprevention, National Cancer Institute, Bethesda, MD 20892, USA.
Wound Repair Regen. 1995 Oct-Dec;3(4):408-18. doi: 10.1046/j.1524-475X.1995.30405.x.
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.
在为加速或改善组织修复而研究的众多生长因子中，没有一种因子的作用谱像转化生长因子-β（TGF-β）那样广泛。自首次描述其促进伤口愈合的能力以来的10年里，在理解其在组织修复中作用的基础方面取得了巨大进展。它从活化的血小板中释放出来，既能作用于参与愈合过程的各种不同细胞类型，也能被这些细胞类型分泌。TGF-β刺激趋化性、纤维生成、血管生成及其表达的自诱导作用，是通过一组独特的丝氨酸-苏氨酸激酶受体进行信号传导介导的，这在机制上使其有别于其他在伤口愈合中有活性的生长因子。在正常愈合和愈合受损的各种动物模型中，无论是在皮肤部位还是在非皮肤部位如骨骼、肠道、眼睛或口腔，局部和全身给予TGF-β均已显示能改善愈合。
