Introduction

Coronary artery disease (CAD), the most common form of cardiovascular disease (CVD), is one of the main causes of mortality and morbidity worldwide [1]. Atherosclerosis, the leading cause of CAD, is a chronic inflammatory disorder with lipid deposition in coronary arteries that in turn develop angina pectoris, myocardial infarction (MI), and death [2].

Genetic and environmental factors such as poor diet, a family history of CAD, aging, smoking, hypertension, diabetes, and dyslipidemia are considered as risk factors for CAD. Dyslipidemia, as a key predictor of atherosclerotic cardiovascular disease, is defined as an increase in plasma total cholesterol (TC), triglyceride (TG), low-density lipoprotein-cholesterol (LDL-C), and decrease in high-density lipoprotein-cholesterol (HDL-C) [3]. CAD is treated mainly through lifestyle changes, such as exercising, eating a healthy diet, and controlling body weight. In some cases, the use of drugs that lower cholesterol and blood pressure, as well as beta blockers and aspirin are also prescribed [4].

The inverse association between HDL-C and CVD risk is well established [

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The data are available from the corresponding author on reasonable request.

Abbreviations

ABCA1/G1:

ATP-binding cassette transporters A1/G1

CAD:

Coronary artery disease

MS-PCR:

Methylation-specific polymerase chain reaction

CVD:

Cardiovascular disease

MI:

Myocardial infarction

TC:

Total cholesterol

TG:

Triglyceride

LDL-C:

Low-density lipoprotein-cholesterol

HDL-C:

High-density lipoprotein-cholesterol

ApoA1:

Apolipoprotein A1

ABC:

ATP-binding cassette

FH:

Familial hypercholesterolemia

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Acknowledgements

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Funding

This research has been funded by the Hormozgan University of medical sciences.

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Author notes

  1. Elaheh Mansouri and Fataneh Esmaeili have equally contributed as first authors

Authors and Affiliations

  1. Molecular Medicine Research Center, Hormozgan Health Institute, Hormozgan University of Medical Sciences, Bandar Abbas, Iran

    Elaheh Mansouri, Fataneh Esmaeili, Shabnaz Koochakkhani, Mahmood Khayatian & Habibollah Turki

  2. Department of Clinical Biochemistry, Faculty of Medicine, Tehran University of Medical Sciences, Tehran, Iran

    Fataneh Esmaeili

  3. School of Health, Kermanshah University of Medical Sciences, Kermanshah, Iran

    Maryam Montaseri

  4. Cardiovascular Research Center, Hormozgan University of Medical Sciences, Bandar Abbas, Iran

    Mohammad Amin Emami

  5. Endocrinology and Metabolism Research Center, Hormozgan University of Medical Sciences, Bandar Abbas, Iran

    Hasan Zarei & Ebrahim Eftekhar

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Contributions

EM was involved in data collection, and performed the experiment. FE helped in data collection, performed the experiment, analyzed the data, and wrote the manuscript. MM analyzed the data; MA E studied conception or design. SK performed the experiment, and wrote the manuscript. MK studied conception or design. HZ studied conception or design. HT studied conception or design. EE contributed to supervision, studied conception or design, helped in critical revision or editing of the article. All authors read and approved the final manuscript.

Corresponding author

Correspondence to Ebrahim Eftekhar.

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This research has been approved by the University Ethics Committee (IR.HUMS.REC.1394.82). All participants were given informed consent and were properly informed of the procedure.

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Mansouri, E., Esmaeili, F., Montaseri, M. et al. Association of methylation status of ABCA1/G1 genes with the risk of coronary artery disease. Egypt J Med Hum Genet 23, 167 (2022). https://doi.org/10.1186/s43042-022-00381-y

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