Department of Cardiology, Xiangyang Central Hospital, Affiliated Hospital of Hubei University of Arts and Science, Xiangyang, Hubei, P.R. China.
PLoS One. 2020 Jun 30;15(6):e0225173. doi: 10.1371/journal.pone.0225173. eCollection 2020.
Vascular hyperplasia after vascular trauma is one of the difficult problems in clinical treatment. Nowadays, there is no effective treatment for vascular hyperplasia. Previous studies have shown that integrinβ1 andβ3 activity play an important role in vascular hyperplasia. Kindlin-2 has been shown to modulate integrinβ1 andβ3 activity in cancer. Therefore, in this study, we hope to explore the relationship between Kindlin-2 and vascular hyperplasia. We overexpressed or knocked down Kindlin-2 by adenovirus. The results showed that Kindlin-2 overexpression could regulate integrinβ1 andβ3 activity through FAK-PIK3 signaling pathways ex vivo and in vivo, thereby affecting the proliferation and migration of VSMC, and then it causes the consequences of vascular hyperplasia. Therefore, Our results show that Kindlin-2 may be a potential target for the treatment of vascular hyperplasia.
血管创伤后的血管增生是临床治疗中的难题之一。目前，对于血管增生尚无有效的治疗方法。既往研究表明整合素β1 和β3 的活性在血管增生中发挥重要作用。Kindlin-2 已被证明可调节整合素β1 和β3 在癌症中的活性。因此，在本研究中，我们希望探索 Kindlin-2 与血管增生之间的关系。我们通过腺病毒过表达或敲低 Kindlin-2。结果表明，Kindlin-2 过表达可通过 FAK-PIK3 信号通路在体外和体内调节整合素β1 和β3 的活性，从而影响 VSMC 的增殖和迁移，进而导致血管增生的后果。因此，我们的结果表明 Kindlin-2 可能是治疗血管增生的潜在靶点。
