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Association of lipid metabolism-related gene promoter methylation with risk of coronary artery disease

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Abstract

Background:

Coronary artery disease (CAD) is a complex disease that is influenced by environmental and genetic factors. Lipid levels are regarded as a major risk factor for CAD, and epigenetic mechanisms might be involved in the regulation of CAD development. This study was designed to investigate the association between the DNA methylation status of 8 lipid metabolism-related genes and the risk of CAD in the Chinese Han population.

Methods:

A total of 260 individuals were sampled in this study, including 120 CAD cases and 140 normal healthy controls. DNA methylation status was tested via targeted bisulfite sequencing.

Results:

The results indicated a significant association between hypomethylation of the APOC3, CETP and APOC1 gene promoters and the risk of CAD. Individuals with higher methylation levels of the APOA5 and LIPC gene promoters had increased risks for CAD. In addition, ANGPTL4 methylation level was significantly associated with CAD in males but not females. There were no significant differences in the methylation levels of the APOB and PCSK9 gene promoters between CAD patients and controls.

Conclusions

The methylation status of the APOC3, APOA5, LIPC, CETP and APOC1 gene promoters may be associated with the development of CAD.

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Acknowledgements

This project was funded by the Shanghai Science and Technology Development Foundation (SY20221RUE01). We also thank Hu Liu from Shanghai Lehao Bio-Science Company for his technical support in gene sequencing.

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Authors and Affiliations

  1. Department of Cardiovascular Surgery, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine, 200127, Shanghai, China

    Wei Li, Yongyi Wang, Ritai Huang, Feng Lian, Genxing Xu, Weijun Wang & Song Xue

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  1. Wei Li
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  5. Genxing Xu
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Correspondence to Song Xue.

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Li, W., Wang, Y., Huang, R. et al. Association of lipid metabolism-related gene promoter methylation with risk of coronary artery disease. Mol Biol Rep 49, 9373–9378 (2022). https://doi.org/10.1007/s11033-022-07789-0

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