National Clinical Research Center for Ocular Diseases, Eye Hospital, Wenzhou Medical University, Wenzhou, 325027, China.
State Key Laboratory of Ophthalmology, Optometry and Visual Science, Eye Hospital, Wenzhou Medical University, Wenzhou, 325027, China.
Eye (Lond). 2023 Oct;37(14):2987-2993. doi: 10.1038/s41433-023-02457-4. Epub 2023 Feb 25.
Pathological myopia (PM) is closely associated with blinding ocular morbidities. Identifying biomarkers can provide clues on pathogeneses. This study aimed to identify metabolic biomarkers and underlying mechanisms in the vitreous humour (VH) of PM patients with complications.
VH samples were collected from 39 PM patients with rhegmatogenous retinal detachment (RRD) (n = 23) or macular hole (MH)/myopic retinoschisis (MRS) (n = 16) and 23 controls (MH with axial length < 26 mm) who underwent surgical treatment. VH metabolomic profiles were investigated using ultra-performance liquid chromatography‒mass spectrometry. The area under the receiver operating characteristic curve (AUC) was computed to identify potential biomarkers for PM diagnosis.
Bioinformatics analysis identified nineteen and four metabolites altered in positive and negative modes, respectively, and these metabolites were involved in tryptophan metabolism. Receiver operating characteristic analysis showed that seventeen metabolites (AUC > 0.6) in the positive mode and uric acid in the negative mode represent potential biomarkers for PM with complications (AUC = 0.894). Pairwise and pathway analyses among the RRD-PM, MH/MRS-PM and control groups showed that tryptophan metabolism and uric acid were closely correlated with PM. Altered metabolites and pathways in our study were characterized by increased oxidative stress and altered energy metabolism. These results contribute to a better understanding of myopia progression with or without related complications.
Our study provides metabolomic signatures and related immunopathological features in the VH of PM patients, revealing new insight into the prevention and treatment of PM and related complications.
病理性近视(PM)与致盲性眼部病变密切相关。寻找生物标志物可以为发病机制提供线索。本研究旨在确定伴有并发症的 PM 患者玻璃体液(VH)中的代谢生物标志物及其潜在机制。
收集了 39 名 PM 伴孔源性视网膜脱离(RRD)(n=23)或黄斑裂孔/高度近视性视网膜劈裂(MRS)(n=16)患者和 23 名接受手术治疗的伴眼轴长度<26mm 的黄斑裂孔对照者(MH)的 VH 样本。采用超高效液相色谱-质谱法检测 VH 代谢组学图谱。计算受试者工作特征曲线(ROC)下面积(AUC)以识别 PM 诊断的潜在生物标志物。
生物信息学分析分别确定了正、负离子模式下改变的 19 种和 4 种代谢物,这些代谢物涉及色氨酸代谢。ROC 分析显示,正离子模式下的 17 种代谢物(AUC>0.6)和负离子模式下的尿酸是 PM 伴并发症的潜在生物标志物(AUC=0.894)。RRD-PM、MH/MRS-PM 和对照组之间的成对和通路分析表明,色氨酸代谢和尿酸与 PM 密切相关。我们研究中改变的代谢物和途径的特征是氧化应激增加和能量代谢改变。这些结果有助于更好地理解近视的进展以及是否伴有相关并发症。
本研究提供了 PM 患者 VH 的代谢组学特征和相关免疫病理特征,为 PM 及相关并发症的防治提供了新的见解。