瘢痕增生瘤是一种良性纤维增生性肿瘤，其特征为过度瘢痕形成。已证实C1q/TNF相关蛋白3（CTRP3）具有抗纤维化作用。在这里，我们探讨了CTRP3在瘢痕增生瘤中的作用。在当前研究中，我们检查了CTRP3对瘢痕增生瘤成纤维细胞（KFs）的影响，并研究了潜在的分子机制。从10例瘢痕增生瘤患者中收集了KF组织标本和相邻的正常成纤维细胞（NF）。对于TGF-β1刺激组，KFs经过人重组TGF-β1处理。进行了pcDNA3.1-CTRP3或pcDNA3.1的细胞转染。CTRP3的siRNA（si-CTRP3）或阴性对照siRNA（si-scramble）被转染到KFs中。CTRP3在瘢痕组织和KFs中被下调。CTRP3过表达明显控制了TGF-β1诱导的KFs的增殖和迁移。TGF-β1刺激增强了Col I、α-SMA和纤维连接蛋白mRNA和蛋白水平，而CTRP3过表达则抑制了它们。相反，CTRP3敲除表现出相反的效应。此外，CTRP3削弱了TGF-β1诱导的KFs的TGF-β受体TRI和TRII。此外，CTRP3防止了TGF-β1刺激的smad2和smad3的核转位，并抑制了KFs中p-smad2和p-smad3的表达水平。CTRP3通过调节TGF-β1/Smad信号通路，在抑制KFs增殖，迁移和ECM累积方面发挥了抗纤维化作用。版权所有© 2023 Lin He等。

Keloid is a type of benign fibrous proliferative tumor characterized by excessive scarring. C1q/TNF-related protein 3 (CTRP3) has been proven to possess antifibrotic effect. Here, we explored the role of CTRP3 in keloid. In the current research, we examined the influence of CTRP3 on keloid fibroblasts (KFs) and investigated the potential molecular mechanism.KF tissue specimens and adjacent normal fibroblast (NF) tissues were collected cultured from 10 keloid participants. For the TGF-β1 stimulation group, KFs were processed with human recombinant TGF-β1. Cell transfection of pcDNA3.1-CTRP3 or pcDNA3.1 was performed. The siRNA of CTRP3 (si-CTRP3) or negative control siRNA (si-scramble) was transfected into KFs.CTRP3 was downregulated in keloid tissues and KFs. CTRP3 overexpression significantly controlled TGF-β1-induced propagation and migration in KFs. Col I, α-SMA, and fibronectin mRNA and protein levels were enhanced by TGF-β1 stimulation, whereas they were inhibited by CTRP3 overexpression. In contrast, CTRP3 knockdown exhibited the opposite effect. In addition, CTRP3 attenuated TGF-β receptors TRI and TRII in TGF-β1-induced KFs. Furthermore, CTRP3 prevented TGF-β1-stimulated nuclear translocation of smad2 and smad3 and suppressed the expression levels of p-smad2 and p-smad3 in KFs.CTRP3 exerted an antifibrotic role through inhibiting proliferation, migration, and ECM accumulation of KFs via regulating TGF-β1/Smad signal path.Copyright © 2023 Lin He et al.