小鼠肺纤维化模型中年龄相关性眼部疾病的诱导。

IF 3 2区 医学 Q1 OPHTHALMOLOGY Experimental eye research Pub Date : 2025-01-10 DOI:10.1016/j.exer.2025.110238
Chao Wang, Xue Li, Qi Tang, Jialu Wu, Jie-Guang Chen
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引用次数: 0

摘要

特发性肺纤维化(IPF)是一种与衰老有关的进行性肺部疾病。本研究利用博莱霉素诱导的 IPF 小鼠模型,探讨了 IPF 与年龄相关眼疾之间的潜在联系。气管内注射博莱霉素会导致小鼠肺部快速损伤,随后出现具有细胞衰老特征的 IPF。IPF损伤小鼠的光斑ERG振幅减小,视觉停滞素免疫染色减弱,表明与杆相关的视觉功能下降。有趣的是,小鼠的眼睛还显示出对金黄色葡萄球菌感染的敏感性增加,这让人联想到衰老的眼睛。为了确定早期衰老是否会导致眼部疾病,我们检测了视网膜中的补体和衰老标记物。在博莱霉素损伤的IPF小鼠中,在感光细胞所在的视网膜核外层发现了DNA损伤相关的衰老标记物γH2AX。此外,IPF 小鼠的 C3b 水平升高,C3b 是一种由 C3 激活产生的补体片段,经常发生在衰老的眼睛中。这些发现强调了 IPF 作为一种有价值的小鼠模型的潜力,可用于研究早期发生的与年龄相关的眼部疾病。
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Induction of age-related ocular disorders in a mouse model of pulmonary fibrosis.

Idiopathic pulmonary fibrosis (IPF) is a progressive lung disease linked to aging. This study investigates potential connections between IPF and age-related eye problems using a bleomycin-induced IPF mouse model. Intratracheal administration of bleomycin induces rapid lung injury in mice, followed by IPF with characteristics of cellular senescence. IPF-injured mice had reduced amplitudes of scotopic ERG and immunostaining of visual arrestin, suggesting declined rod-related visual function. Interestingly, the mice's eyes also showed increased susceptibility to Staphylococcus aureus infections, reminiscent of the aging eyes. To determine whether an early onset of aging contributes to the eye disorders, we examined complement and senescence markers in the retina. In bleomycin-injury IPF mice, DNA damage-related senescence marker γH2AX was found in the retinal out nuclear layer where photoreceptors are located. Additionally, IPF mice displayed elevated levels of C3b, a complement fragment resulting from C3 activation that occurs frequently in aging eyes. These findings underscore the potential of IPF as a valuable mouse model for investigating early-onset age-related ocular disorders.

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来源期刊
Experimental eye research
Experimental eye research 医学-眼科学
CiteScore
6.80
自引率
5.90%
发文量
323
审稿时长
66 days
期刊介绍: The primary goal of Experimental Eye Research is to publish original research papers on all aspects of experimental biology of the eye and ocular tissues that seek to define the mechanisms of normal function and/or disease. Studies of ocular tissues that encompass the disciplines of cell biology, developmental biology, genetics, molecular biology, physiology, biochemistry, biophysics, immunology or microbiology are most welcomed. Manuscripts that are purely clinical or in a surgical area of ophthalmology are not appropriate for submission to Experimental Eye Research and if received will be returned without review.
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