瘢痕疙瘩是皮肤损伤后成纤维细胞过度增生和胶原异常积聚所致的过度瘢痕化，遗传因素在其发病中发挥重要作用，但机制仍未明。我们前期研究发现，瘢痕疙瘩易感位点rs1348270位于增强子上,敲除该增强子显著下调LINC01705的表达，而LINC01705在瘢痕疙瘩中高表达并能调控胶原合成。据此我们提出假说：rs1348270通过增强子调控LINC01705的表达，增强细胞胶原合成促进瘢痕疙瘩发生发展。为验证假说，我们拟以CRISPR/Cas9、ChIP等技术，明确rs1348270调控LINC01705的机理；以细胞和分子生物学方法明确LINC01705在瘢痕疙瘩中的功能和发挥作用的机理；以基因测序、荧光原位杂交等方法明确rs1348270和LINC01705在瘢痕疙瘩中的临床意义。该研究将揭示rs1348270通过LINC01705影响瘢痕疙瘩发生发展的机理，对瘢痕疙瘩临床诊疗具有重要意义。

Keloid represents one extreme of aberrant dermal wound healing and is characterized by fibroblast abnormal proliferation and excessive deposition of collagen. Genetic factors play an important role in its pathogenesis, but its regulatory mechanism remains unclear. In preliminary study, we found that the keloid susceptibility site rs1348270 is located on the enhancer, Knock-out of the enhancer down regulated the expression of LINC01705, and LINC01705 was high expressed in keloid and could regulate the collagen synthesis. Based on these findings, we hypothesize that rs1348270 may regulate the expression of LINC01705 through enhancer, and up-regulate the expression of collagen to promote the formation and development of keloid. To verify the hypothesis, we will explore the mechanism that rs1348270 regulates LINC01705 by using experiments such as CRISPR/Cas9 and ChIP. Next we will use cell and molecular biology methods to clarify the function and mechanism of LINC01705 in keloid. At last we will use experiments such as gene sequencing and FISH to study the clinical significance of rs1348270 and LINC01705 in keloid. This study will reveal the mechanism of rs1348270 influencing the formation and development of keloid through LINC01705, which is of great significance for clinical diagnosis and treatment of keloid.