Keloids are benign skin tumors characterized by aggressive growth. To date, there is no exact treatment because little is known about its pathological mechanism. Therefore, it is important to investigate the mechanism of its occurrence and development to identify therapeutic targets. In this study, the expression of Kindlin-2 was higher in keloid fibroblasts (KFs) than in normal skin fibroblasts (NFs). In vitro experiments showed that knocking down Kindlin-2 in KFs could promote cell apoptosis and inhibit cell proliferation, cell migration and invasion, and contractile capability. Western blot results showed that the phosphorylation of Smad3 in KFs was inhibited after knocking down Kindlin-2, inhibiting the activation of the Smad pathway. Moreover, knocking down Kindlin-2 increased the expression of Fas and FasL in KFs, which demonstrated that knocking down Kindlin-2 promoted the activation of the exogenous apoptotic pathway of KFs and then facilitated apoptosis. The above results revealed that knocking down Kindlin-2 in KFs can inhibit the activation of the Smad pathway and promote the activation of the Fas/FasL exogenous apoptosis pathway, thereby altering the cytological function of KFs. Therefore, Kindlin-2 might play an important role in the occurrence and development of keloids and could become a new target to treat keloids.

瘢痕疙瘩是一种以侵袭性生长为特征的良性皮肤肿瘤。迄今为止，尚无确切的治疗方法，因为对其病理机制知之甚少。因此，研究其发生和发展的机制以确定治疗靶点很重要。在这项研究中，Kindlin-2 在瘢痕疙瘩成纤维细胞 (KFs) 中的表达高于在正常皮肤成纤维细胞 (NFs) 中的表达。体外实验表明，敲低KFs中的Kindlin-2可促进细胞凋亡，抑制细胞增殖、细胞迁移和侵袭以及收缩能力。Western blot结果表明，KFs中Smad3的磷酸化在敲低Kindlin-2后受到抑制，抑制了Smad通路的激活。此外，敲低 Kindlin-2 增加了 KFs 中 Fas 和 FasL 的表达，这表明敲低 Kindlin-2 促进了 KFs 外源性凋亡途径的激活，进而促进了细胞凋亡。以上结果表明，敲低KFs中的Kindlin-2可以抑制Smad通路的激活，促进Fas/FasL外源性凋亡通路的激活，从而改变KFs的细胞学功能。因此，Kindlin-2可能在瘢痕疙瘩的发生发展中起重要作用，有望成为治疗瘢痕疙瘩的新靶点。从而改变 KFs 的细胞学功能。因此，Kindlin-2可能在瘢痕疙瘩的发生发展中起重要作用，有望成为治疗瘢痕疙瘩的新靶点。从而改变 KFs 的细胞学功能。因此，Kindlin-2可能在瘢痕疙瘩的发生发展中起重要作用，有望成为治疗瘢痕疙瘩的新靶点。