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Published on: August 8, 2022
HMOX1 gene promoter polymorphism is not associated with coronary artery disease in Koreans
Seong Woo Han1, Wonkeun Song2, Han-Sung Kim2
1Department of Cardiology, Hallym University College of Medicine, Seoul, Korea.
Insights
Heme oxygenase-1 (HMOX1) gene polymorphisms are not linked to coronary artery disease (CAD) in Koreans. However, carriers of the short HMOX1 allele showed lower high-sensitivity C-reactive protein levels, indicating reduced cardiovascular risk.
Area of Science:
- Genetics
- Cardiovascular Disease
- Molecular Biology
Background:
- Heme oxygenase-1 (HMOX1) gene polymorphisms influence gene transcription in response to oxidative stress.
- Investigating the association between HMOX1 polymorphisms and coronary artery disease (CAD) is crucial for understanding disease mechanisms.
Purpose of the Study:
- To screen for HMOX1 polymorphisms.
- To investigate the association between HMOX1 polymorphisms and CAD in the Korean population.
Main Methods:
- Study population included 110 CAD patients with obstructive lesions, 40 with minimal/no lesions, and 107 controls.
- PCR analysis of the 5'-flanking region containing (GT)n repeats of the HMOX1 gene.
- Follow-up coronary angiography in 39 CAD patients to assess restenosis.
Main Results:
- HMOX1 (GT)n repeats showed a bimodal distribution, categorized into S25 (≤25 repeats) and L25 (>25 repeats) alleles.
- No statistically significant differences in allele or genotype frequencies were observed among CAD and control groups.
- S25 allele carriers had significantly lower high-sensitivity C-reactive protein (hsCRP) levels compared to non-carriers (P=0.034).
Conclusions:
- HMOX1 genotypes were not associated with CAD in the Korean population.
- Carriers of the short (S25) HMOX1 allele exhibited hsCRP levels indicative of a lower cardiovascular disease risk.
- Further research may explore the protective role of the S25 allele in cardiovascular health.
Background:
The heme oxygenase-1 gene (HMOX1) promoter polymorphisms modulate its transcription in response to oxidative stress. This study screened for HMOX1 polymorphisms and investigated the association between HMOX1 polymorphisms and coronary artery disease (CAD) in the Korean population.
Methods:
The study population consisted of patients with CAD with obstructive lesions (n=110), CAD with minimal or no lesions (n=40), and controls (n=107). Thirty-nine patients with CAD with obstructive lesions underwent follow-up coronary angiography after six months for the presence of restenosis. The 5'-flanking region containing (GT)n repeats of the HMOX1 gene was analyzed by PCR.
Results:
The numbers of (GT)n repeats in the HMOX1 promoter showed a bimodal distribution. The alleles were divided into two subclasses, S25 and L25, depending on whether there were less than or equal to and more than 25 (GT)n repeats, respectively. The allele and genotype frequencies among groups were statistically not different. More subjects in the S25-carrier group had the low risk levels of high sensitivity C-reactive protein (hsCRP) for the CAD than those in the non-S25 carrier group (P=0.034). Multivariate logistic regression analysis revealed that the genotypes of (GT)n repeats were not related to CAD status. The restenosis group in the coronary angiography follow-up did not show any significant difference in HMOX1 genotype frequency.
Conclusions:
The HMOX1 genotypes were not found to be associated with CAD, but the short allele carrier group contained more individuals with hsCRP values reflecting low risk of cardiovascular disease in the Korean population.
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