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Background <p>Observational studies have identified a possible connection between lipid-lowering medications and respiratory illnesses. However, it remains unclear whether lipid-lowering drugs is causative for respiratory diseases, and we aimed to answer this question.</p> Methods <p>We performed Mendelian randomization (MR) analyses by integrating data from genome-wide association studies (GWAS). Three statistical approaches were employed for MR analysis: inverse variance weighting (IVW), MR-Egger, and weighted median. The purpose was to evaluate the causal relationships between 10 drug targets that lower lipid levels and the likelihood of developing 7 respiratory diseases. Additional sensitivity analyses were conducted to ensure the robustness and validity of the results.</p> Results <p>After adjusting for multiple testing, our MR analysis identified APOB (odd ratios [OR]: 0.86; 95% confidence interval [CI]: 0.77 to 0.97; P<sub>IVW</sub> = 0.01) and PCSK9 (OR: 0.84; 95% CI: 0.72 to 0.97; P<sub>IVW</sub> = 0.02) as significant risk targets for asthma. Additionally, LDLR was found to be a significant risk target for chronic obstructive pulmonary disease (OR: 0.81; 95% CI: 0.67 to 0.98; P<sub>IVW</sub> = 0.03). The sensitivity analysis validated no proof of heterogeneity or pleiotropy amongst the mentioned results.</p> Conclusions <p>Our findings suggest a likely causal relationship between respiratory diseases and lipid-lowering drug targets. Further mechanistic and clinical research is needed to confirm and validate these findings.</p>

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Lipid-lowering drug targets associated with risk of respiratory disease: a Mendelian randomization study

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年2月11日

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  • Zhipeng Gong,
  • Dongsheng Wu,
  • Yin Ku,
  • Congyao Zou,
  • Lin Qiu,
  • Xiaohu Hao,
  • Lunxu Liu

摘要

Background

Observational studies have identified a possible connection between lipid-lowering medications and respiratory illnesses. However, it remains unclear whether lipid-lowering drugs is causative for respiratory diseases, and we aimed to answer this question.

Methods

We performed Mendelian randomization (MR) analyses by integrating data from genome-wide association studies (GWAS). Three statistical approaches were employed for MR analysis: inverse variance weighting (IVW), MR-Egger, and weighted median. The purpose was to evaluate the causal relationships between 10 drug targets that lower lipid levels and the likelihood of developing 7 respiratory diseases. Additional sensitivity analyses were conducted to ensure the robustness and validity of the results.

Results

After adjusting for multiple testing, our MR analysis identified APOB (odd ratios [OR]: 0.86; 95% confidence interval [CI]: 0.77 to 0.97; PIVW = 0.01) and PCSK9 (OR: 0.84; 95% CI: 0.72 to 0.97; PIVW = 0.02) as significant risk targets for asthma. Additionally, LDLR was found to be a significant risk target for chronic obstructive pulmonary disease (OR: 0.81; 95% CI: 0.67 to 0.98; PIVW = 0.03). The sensitivity analysis validated no proof of heterogeneity or pleiotropy amongst the mentioned results.

Conclusions

Our findings suggest a likely causal relationship between respiratory diseases and lipid-lowering drug targets. Further mechanistic and clinical research is needed to confirm and validate these findings.