PDF(Pubmed)
Abstract：
Hypoxia-inducible factor (HIF) plays a crucial role in regulating oxygen sensing and adaptation at the cellular level, overseeing cellular oxygen homeostasis, erythrocyte production, angiogenesis, and mitochondrial metabolism. The hypoxia-sensitive HIF-1α subunit facilitates tissue adaptation to hypoxic conditions, including the stimulation of proangiogenic factors. Retinopathy of prematurity (ROP) is a proliferative vascular disease of the retina that poses a significant risk to prematurely born children. If untreated, ROP can lead to retinal detachment, severe visual impairment, and even blindness. The pathogenesis of ROP is not fully understood; however, reports suggest that premature birth leads to the exposure of immature ocular tissues to high levels of exogenous oxygen and hyperoxia, which increase the synthesis of reactive oxygen species and inhibit HIF expression. During the ischemic phase, HIF-1α expression is stimulated in the hypoxia-sensitive retina, causing an overproduction of proangiogenic factors and the development of pathological neovascularization. Given the significant role of HIF-1α in the development of ROP, considering it as a potential molecular target for therapeutic strategies appears justified. This review synthesizes information from the last six years (2018-2024) using databases such as PubMed, Google Scholar, and BASE, focusing on the role of HIF-1α in the pathogenesis of ROP and its potential as a target for new therapies.
摘要：
缺氧诱导因子（HIF）在调节细胞水平的氧敏感和适应中起着至关重要的作用。监督细胞氧稳态，红细胞产生，血管生成,和线粒体代谢.缺氧敏感性HIF-1α亚基促进组织适应缺氧条件，包括刺激促血管生成因子。早产儿视网膜病（ROP）是视网膜的增生性血管疾病，对早产儿童构成重大风险。如果未经治疗,ROP会导致视网膜脱离,严重的视力障碍，甚至失明。ROP的发病机制尚不完全清楚；然而，报告表明，早产导致未成熟的眼组织暴露于高水平的外源性氧气和高氧，增加活性氧的合成并抑制HIF的表达。在缺血期,缺氧敏感性视网膜中HIF-1α的表达受到刺激,导致促血管生成因子的过度产生和病理性新生血管的发展。鉴于HIF-1α在ROP发生发展中的重要作用,将其视为治疗策略的潜在分子靶标似乎是合理的.这篇综述使用PubMed、谷歌学者，和基地，重点关注HIF-1α在ROP发病机制中的作用及其作为新疗法靶点的潜力。
