New advances in pharmacological research for retinopathy of prematurity.

Q2 Medicine
Yanxi Xie, Suilian Zheng, Hui Yang
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引用次数: 0

Abstract

Retinopathy of prematurity (ROP) is a proliferative retinal vascular disease that threatens the vision of premature infants. Various novel drugs have demonstrated therapeutic potential for ROP by targeting signaling pathways associated with vascular endothelial growth factor (VEGF), including PI3K/AKT, hypoxia-inducible factor (HIF)-1α/VEGF, oxidative stress, tumor necrosis factor (TNF)-α, and Notch pathways. Propranolol, insulin-like growth factor-1, and celecoxib attenuate pathological neovascularization via the PI3K/AKT signaling pathway. Tripterine and melatonin inhibit retinal neovascularization by modulating the HIF-1α/VEGF signaling axis. Adiponectin mitigates oxidative stress damage and preserves endothelial function by enhancing endothelial nitric oxide synthase activity. Omega-3 polyunsaturated fatty acids suppress TNF-α-mediated inflammatory responses, modulate retinal development and angiogenesis, and reduce retinal neovascular lesions. The γ-secretase inhibitor DAPT blocks Notch signaling to suppress abnormal vascular proliferation. These agents exhibit synergistic multi-pathway anti-angiogenic effects in preclinical models and early-phase clinical trials, offering critical insights for advancing drug development and clinical translation in ROP management.

早产儿视网膜病变的药理研究新进展。
早产儿视网膜病变(ROP)是一种威胁早产儿视力的增殖性视网膜血管疾病。多种新药通过靶向与血管内皮生长因子(VEGF)相关的信号通路,包括PI3K/AKT、缺氧诱导因子(HIF)-1α/VEGF、氧化应激、肿瘤坏死因子(TNF)-α和Notch通路,显示出治疗ROP的潜力。心得安、胰岛素样生长因子-1和塞来昔布通过PI3K/AKT信号通路减弱病理性新生血管。雷公藤红素和褪黑素通过调节HIF-1α/VEGF信号轴抑制视网膜新生血管。脂联素通过增强内皮一氧化氮合酶活性,减轻氧化应激损伤,保护内皮功能。Omega-3多不饱和脂肪酸抑制TNF-α介导的炎症反应,调节视网膜发育和血管生成,减少视网膜新生血管病变。γ-分泌酶抑制剂DAPT阻断Notch信号,抑制血管异常增殖。这些药物在临床前模型和早期临床试验中表现出协同的多途径抗血管生成作用,为推进药物开发和ROP管理的临床转化提供了重要见解。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
CiteScore
3.80
自引率
0.00%
发文量
67
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