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纳米硅酸盐通过激活活性氧介导的WNT/β-连环蛋白信号通路促进血管生成。

Nanosilicates promote angiogenesis through activation of ROS-mediated WNT/β-catenin pathway.

作者信息

Lokhande Giriraj, Singh Kanwar Abhay, Roy Shounak, Soukar John, Kersey Anna, Borkar Pranita, Biswas Saptarshi, Syed Raza Ur Rehman, Keller Anna, Bayless Kayla J, Singh Irtisha, Gaharwar Akhilesh K

机构信息

Department of Biomedical Engineering, College of Engineering, Texas A&M University, College Station, TX 77843, USA.

Department of Cell Biology and Genetics, College of Medicine, Texas A&M University, Bryan, TX 77807, USA.

出版信息

Sci Adv. 2025 Jul 4;11(27):eado1223. doi: 10.1126/sciadv.ado1223. Epub 2025 Jul 2.

Abstract

Scaffold vascularization plays a pivotal role in the wound healing process, facilitating the recruitment of endogenous progenitor cells and delivering crucial signaling molecules that promote cellular invasion, angiogenesis, and neotissue formation. In this study, we introduce nanosilicates as proangiogenic biomaterials that can prime endogenous cells to expedite angiogenesis and graft vascularization in vivo. Characterized by their mineral-based two-dimensional structure and extensive surface area, nanosilicates are efficiently internalized by endothelial cells, leading to augmented cellular migration and the formation of tubular structures. Through whole transcriptome sequencing, we elucidated that nanosilicates activate the canonical Wnt pathway through hypoxia-induced ROS production. In vivo investigations further corroborate the proangiogenic efficacy of nanosilicate-loaded biomaterials. This study posits nanosilicates as a potential proangiogenic adjunct in the design of biomaterials for in situ tissue regeneration.

摘要

支架血管化在伤口愈合过程中起着关键作用,有助于募集内源性祖细胞并传递促进细胞侵袭、血管生成和新组织形成的关键信号分子。在本研究中,我们引入纳米硅酸盐作为促血管生成生物材料,其可激发内源性细胞以加速体内血管生成和移植组织血管化。纳米硅酸盐具有基于矿物的二维结构和较大的表面积,能被内皮细胞有效内化,从而增强细胞迁移并形成管状结构。通过全转录组测序,我们阐明纳米硅酸盐通过缺氧诱导的活性氧生成激活经典Wnt通路。体内研究进一步证实了负载纳米硅酸盐的生物材料的促血管生成功效。本研究将纳米硅酸盐定位为用于原位组织再生的生物材料设计中的一种潜在促血管生成辅助材料。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c5af/12219486/a4faf1d2f4d1/sciadv.ado1223-f1.jpg

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