孟德尔随机化
医学
感音神经性聋
遗传学
SOD2
听力损失
生物信息学
听力学
生物
基因
内科学
超氧化物歧化酶
基因型
氧化应激
遗传变异
作者
Jiangyu Yan,Linrong Wu,Mengmeng Zheng,Yuan Lv,Feng Jiang,Weibo Gao,Fangfang Pan
出处
期刊:Otology & Neurotology
[Ovid Technologies (Wolters Kluwer)]
日期:2024-07-25
标识
DOI:10.1097/mao.0000000000004266
摘要
Background Mitochondrial proteins assume a pivotal role in the onset and progression of diverse diseases. Nonetheless, the causal interconnections with sensorineural hearing loss (SNHL) demand meticulous exploration. Mendelian randomization analysis is a method used in observational epidemiological studies to predict the relationship between exposure factors and outcomes using genetic variants as instrumental variables. In this study, we applied this analytical approach to two distinct samples to predict the causal impact of mitochondrial proteins on SNHL. Methods Two-sample Mendelian randomization analyses were executed to scrutinize the predicted associations between 63 mitochondrial proteins (nuclear-encoded) and SNHL, utilizing summary statistics derived from genome-wide association studies. Assessments of pleiotropy and heterogeneity were carried out to gauge the robustness of the obtained findings. Results Four mitochondrial proteins exhibited a suggestive causal relationship with the susceptibility to SNHL. Dihydrolipoamide dehydrogenase (DLD; OR = 0.9706, 95% CI = 0.9382–0.9953, p = 0.0230) was linked to a diminished risk of SNHL. Conversely, elevated levels of mitochondrial ribosomal protein L34 (MRPL34; OR = 1.0458, 95% CI = 1.0029–1.0906, p = 0.0362), single-pass membrane protein with aspartate-rich tail 1 (SMDT1; OR = 1.0619, 95% CI = 1.0142–1.1119, p = 0.0104), and superoxide dismutase 2 (SOD2; OR = 1.0323, 95% CI = 1.0020–1.0634, p = 0.0364) were associated with an elevated risk of SNHL. Conclusion This research utilized Mendelian randomization analysis to predict the relationship between mitochondrial proteins and SNHL. It provides a potential viewpoint on the etiology and diagnosis.
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