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烧伤后瘢痕增生机制较复杂,是在遗传、细胞因子、生物化学因子、创伤修复等多种因素共同作用的结果。p53基因与瘢痕增生关系研究相对透彻,基因突变与病理性瘢痕关系密切,p53基因第78密码子SNp位点CCC基因型可能是瘢痕的易感基因。肿瘤坏死因子(TNF)、表皮生长因子(EGF)、转化生长因子(TGF-β)、血管内皮生长因子(VEGF)等构成庞大的细胞因子网络参与瘢痕发生进展,通过影响成纤维细胞等细胞分化、增生、细胞外机制分泌、瘢痕微血管形成等途径影响瘢痕增生。脯氨酸羟化酶胶原、胶原纤维等通过影响胶原合成与排列影响瘢痕增生。烧伤的深度、严重程度通过影响修复进程影响瘢痕增生。
Burn scar hypertrophy mechanism is more complex, is in the genetic, cytokines, biochemical factors, wound repair and many other factors result. The relationship between p53 gene and scar hyperplasia is relatively thorough, and the gene mutation is closely related to pathological scar. CCC genotype at the SNp site of codon 78 of p53 gene may be a susceptible gene to scar. Tumor necrosis factor (TNF), epidermal growth factor (EGF), transforming growth factor (TGF-β), vascular endothelial growth factor (VEGF) constitute a large network of cytokines involved in the progress of scarring, through the influence of fibroblasts and other cell differentiation , Hyperplasia, extracellular mechanism of secretion, scar formation and other means of scar hyperplasia. Proline hydroxylase collagen, collagen fibers affect the collagen synthesis and arrangement of scar hyperplasia. The depth and severity of burns affect scarring by affecting the healing process.