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Hypercholesterolemia as a Causal Risk Factor for COPD: Biomarker Discovery and Therapeutic Implications From NHANES Data
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DOI：10.2147/COPD.S526511.png)
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Abstract
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Lu Liu,1,2,* Chaoling Wu,1,* Zhiyan Zhang,3 Xinxing Jin,4 Qi Zou,5 Mingxue Wang,1 Bo Huang,1 Xin Gan,2 Jianlin Tong1 1Department of Respiratory Medicine, Affiliated Hospital of Jiujiang University, Jiujiang, 332000, People’s Republic of China; 2Department of Respiratory and Critical Care, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi Province, 330006, People’s Republic of China; 3Jiangxi Institute of Respiratory Disease, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi Province, 330006, People’s Republic of China; 4Department of Respiratory and Critical Care, Gaoxin Hospital of the First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi Province, 330006, People’s Republic of China; 5Department of Geriatric Medicine, Affiliated Hospital of Jiujiang University, Jiujiang, 332000, People’s Republic of China *These authors contributed equally to this work Correspondence: Xin Gan, Department of Respiratory and Critical Care, The First Affiliated Hospital of Nanchang University, 17 Yong Waizheng Street, Donghu District, Nanchang, Jiangxi Province, 330006, People’s Republic of China, Email ganxin1207@126.com Jianlin Tong, Department of Respiratory medicine, Affiliated Hospital of Jiujiang University, No. 57 East Xunyang Road, Xunyang District, Jiujiang, 332000, People’s Republic of China, Email tjl8880@163.com Background: Chronic obstructive pulmonary disease (COPD), the third leading cause of global mortality, imposes substantial socioeconomic burdens. Existing therapies, such as smoking cessation and non-invasive ventilation, primarily alleviate symptoms without arresting disease progression. Comorbidities, including cardiovascular disease and metabolic syndrome, exacerbate functional decline, yet the causal role of dyslipidemia in COPD pathogenesis remains unclear. This study seeks to establish a causal link between hypercholesterolemia and COPD while identifying potential biomarkers and therapeutic targets. Methods: Leveraging cross-sectional data from the National Health and Nutrition Examination Survey (NHANES), we employed Mendelian randomization (MR) analysis using 71 single-nucleotide polymorphisms (SNPs) associated with hypercholesterolemia, integrated with bioinformatics tools for Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses. Demographic variables (age, sex, body mass index [BMI]) and dietary factors were compared between COPD patients and controls. Results: Univariate analyses identified significant differences in demographics and dietary patterns between COPD and non-COPD groups (P < 0.05). Multivariate logistic regression revealed: (1) a reduced risk of COPD with elevated total cholesterol levels (odds ratio [OR]: 0.815, 95% confidence interval [CI]: 0.721– 0.923, P = 0.001); and (2) increased COPD risk associated with higher age and BMI. Bioinformatics analyses pinpointed atorvastatin, fenofibrate, and pravastatin as candidate therapeutics. Gene interaction networks and pathway enrichment highlighted roles for lipid homeostasis and cholesterol metabolism. Conclusion: Analysis of NHANES data demonstrates an inverse association between cholesterol levels and COPD prevalence, with MR confirming a causal relationship. These findings underscore targetable pathways and suggest repurposing statins and fibrates, meriting further mechanistic studies and clinical trials for validation. Keywords: COPD, Mendelian randomization, NHANES, HMGCR
Keywords:
COPD
Mendelian randomization
NHANES
HMGCR
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