Genetic variations in circadian rhythm genes and susceptibility for myocardial infarction.
Ivana SkrlecJakov MilicMarija HefferBorut PeterlinJasenka WagnerPublished in: Genetics and molecular biology (2018)
Disruption of endogenous circadian rhythms has been shown to increase the risk of developing myocardial infarction (MI), suggesting that circadian genes might play a role in determining disease susceptibility. We conducted a case-control study on 200 patients hospitalized due to MI and 200 healthy controls, investigating the association between MI and single nucleotide polymorphisms (SNPs) in four circadian genes (ARNTL, CLOCK, CRY2, and PER2). The variants of all four genes were chosen based on their previously reported association with cardiovascular risk factors, which have a major influence on the occurrence of myocardial infarction. Statistically significant differences, assessed through Chi-square analysis, were found in genotype distribution between cases and controls of the PER2 gene rs35333999 (p=0.024) and the CRY2 gene rs2292912 (p=0.028); the corresponding unadjusted odds ratios, also significant, were respectively OR=0.49 (95% CI 0.26-0.91) and OR=0.32 (95% CI 0.11-0.89). Our data suggest that genetic variability in the CRY2 and PER2 genes might be associated with myocardial infarction.
Keyphrases
- genome wide
- genome wide identification
- copy number
- dna methylation
- heart failure
- cardiovascular risk factors
- left ventricular
- genome wide analysis
- newly diagnosed
- electronic health record
- cardiovascular disease
- metabolic syndrome
- gene expression
- machine learning
- risk assessment
- prognostic factors
- heart rate
- patient reported outcomes
- big data
- peritoneal dialysis