Ke Chaofu, Xu Hua, Chen Qin, Zhong Hua, Pan Chen-Wei
School of Public Health, Medical College of Soochow University, Suzhou, China.
Department of Ophthalmology, Children's Hospital of Soochow University, Suzhou, China.
Eye (Lond). 2021 Mar;35(3):817-824. doi: 10.1038/s41433-020-0968-z. Epub 2020 May 18.
High myopia is associated with blinding ocular morbidities. Identifying novel biomarkers may provide clues on pathogenic pathways that are currently unknown. We aimed to identify serum metabolic biomarkers and investigate the metabolic alterations in relation to high myopia.
Forty adults with high myopia and 40 with low myopia aged 60 years or older from the Weitang Geriatric Diseases study were included in the case-control study. Refractive error was determined by autorefraction followed by subjective refraction. We performed the metabolomic analysis of serum samples from patients with high myopia and age- and sex- matched controls with low myopia, using a nontargeted gas chromatography coupled to time-of-flight mass spectrometer. The area under the receiver operating characteristic curve (AUC) was computed to assess the discrimination capacities of each metabolite marker. Databases including KEGG and MetaboAnalyst were utilized to search for the potential pathways of metabolites.
Serum metabolomic profiles could well distinguish high myopia from low myopia. Twenty metabolic biomarkers were identified as potential serum biomarkers for high myopia, yielding AUC values of 0.59-0.71. Metabolic pathways in relation to high myopia, mainly characterized by increased energy metabolism, increased oxidative stress, abnormal amino acid metabolism, and altered biotin metabolism, provide a foundation to support myopia progression.
This study identified valuable metabolic biomarkers and pathways that may facilitate an improved understanding of the disease pathogenesis. The finding holds translational value in the development of new therapeutic measures for high myopia-related complications.
高度近视与致盲性眼部疾病相关。识别新的生物标志物可能为目前未知的致病途径提供线索。我们旨在识别血清代谢生物标志物,并研究与高度近视相关的代谢改变。
来自渭塘老年疾病研究的40名60岁及以上的高度近视成年人和40名低度近视成年人被纳入病例对照研究。通过自动验光然后主观验光来确定屈光不正。我们使用非靶向气相色谱-飞行时间质谱仪对高度近视患者和年龄及性别匹配的低度近视对照者的血清样本进行代谢组学分析。计算受试者工作特征曲线(AUC)下的面积以评估每个代谢物标志物的辨别能力。利用包括KEGG和MetaboAnalyst在内的数据库来搜索代谢物的潜在途径。
血清代谢组学谱能够很好地区分高度近视和低度近视。20种代谢生物标志物被确定为高度近视的潜在血清生物标志物,AUC值为0.59 - 0.71。与高度近视相关的代谢途径,主要表现为能量代谢增加、氧化应激增加、氨基酸代谢异常和生物素代谢改变,为支持近视进展提供了基础。
本研究识别出了有价值的代谢生物标志物和途径,可能有助于更好地理解疾病发病机制。这一发现对于开发高度近视相关并发症的新治疗措施具有转化价值。