Yuan Chao-Yi, Zuo Ling, Dong Yu-Chen, Liu Bao-Xing, Qi Hui
Department of Ophthalmology, The Second Hospital of Jilin University, #218 Ziqiang Street, Changchun, 130041, Jilin, China.
Int Ophthalmol. 2025 Jan 20;45(1):26. doi: 10.1007/s10792-024-03393-2.
The purpose of this study is to investigate the role of Secretogranin III (Scg3) in the pathogenesis of intraocular neovascular diseases and assess its potential as a therapeutic target for novel treatment strategies.
A literature review was conducted to examine the expression of Scg3 in intraocular neovascular diseases. We reviewed studies on the interaction of Scg3 with its homologous receptors and its effect on endothelial cell proliferation, migration, and vascular permeability-key processes involved in angiogenesis and neovascularization.
Scg3 was found to be upregulated in the tissues affected by diabetic retinopathy (DR), retinopathy of prematurity (ROP), and choroidal neovascularization. In DR, Scg3 expression was linked to retinal neovascularization, where it facilitated endothelial cell proliferation and migration, essential processes for the formation of new blood vessels. Similarly, in ROP, Scg3 was associated with fibrovascular tissue proliferation within avascular retinal zones, contributing to the pathological neovascularization seen in premature infants. In the context of age-related macular degeneration (AMD), Scg3 appeared to play a role in choroidal neovascularization, where it promoted the invasion of choroidal capillaries into the retinal pigment epithelium. Furthermore, Scg3's binding to its homologous receptors was shown to enhance vascular permeability, potentially exacerbating fluid leakage and edema in these diseases, which is a hallmark of exudative conditions. Collectively, these findings suggest that Scg3 plays a pivotal role in driving angiogenesis and vascular permeability in intraocular neovascular diseases CONCLUSION: The upregulation of Scg3 in DR, ROP, and choroidal neovascularization highlights its potential as a novel therapeutic target. Inhibition of Scg3 could offer a new avenue for treating these sight-threatening conditions.
本研究旨在探讨分泌粒蛋白III(Scg3)在眼内新生血管疾病发病机制中的作用,并评估其作为新型治疗策略治疗靶点的潜力。
进行文献综述以研究Scg3在眼内新生血管疾病中的表达。我们回顾了关于Scg3与其同源受体相互作用及其对内皮细胞增殖、迁移和血管通透性(血管生成和新生血管形成中的关键过程)影响的研究。
发现Scg3在糖尿病性视网膜病变(DR)、早产儿视网膜病变(ROP)和脉络膜新生血管形成所累及的组织中表达上调。在DR中,Scg3的表达与视网膜新生血管形成相关,它促进内皮细胞增殖和迁移,这是新血管形成的关键过程。同样,在ROP中,Scg3与无血管视网膜区域内的纤维血管组织增殖有关,导致早产儿出现病理性新生血管形成。在年龄相关性黄斑变性(AMD)的背景下,Scg3似乎在脉络膜新生血管形成中起作用,它促进脉络膜毛细血管侵入视网膜色素上皮。此外,已表明Scg3与其同源受体的结合会增强血管通透性,可能会加剧这些疾病中的液体渗漏和水肿,这是渗出性疾病的一个标志。总的来说,这些发现表明Scg3在眼内新生血管疾病中驱动血管生成和血管通透性方面起关键作用。结论:Scg3在DR、ROP和脉络膜新生血管形成中的上调突出了其作为新型治疗靶点的潜力。抑制Scg3可为治疗这些威胁视力的疾病提供新途径。