Key result
PEAR1 genetic variation shows no link to incident hypertension over 10 years.
Why the study?
PEAR1 was identified as a candidate gene linked to blood-pressure driven kidney injury in salt-sensitive rats, but its association with blood pressure or hypertension in humans was unclear.
Is genetic variation in the PEAR1 gene associated with changes in blood pressure or incidence of hypertension in a European population?
Cohort (n=1,973)
Is genetic variation in the PEAR1 gene associated with changes in blood pressure or incidence of hypertension in a European population?
Hazard Ratio: 1.09
p-value: p=≥ 0.09
Genetic variation in the PEAR1 gene is not associated with blood pressure changes or hypertension incidence in humans, challenging experimental findings in animal models.
PEAR1 variants associated with BP changes or hypertension incidence; extends candidate gene data but leaves open causal validation in diverse cohorts.
OBJECTIVE: Platelet endothelial aggregation receptor 1 (PEAR1) is a membrane protein involved in platelet contact-induced activation and sustained platelet aggregation. Experimental studies identified PEAR1, as a candidate gene that may be linked to the blood-pressure driven kidney injury in salt-sensitive Dahl rats. AIM: In a family-based European population study (mean age 39.7 years; 52.2% women), we searched for association of changes in blood pressure or incidence of hypertension with genetic variation in PEAR1. METHODS: Among 1973 randomly recruited people, genotyped for PEAR1, we measured blood pressure at baseline and follow-up. RESULTS: Median follow-up was 10.0 years. While accounting for family clusters and blood pressure at baseline and with adjustments applied for sex, age, body mass index, smoking and drinking, total cholesterol, and antihypertensive drug treatment, all associations of systolic and diastolic blood pressure changes with nine single nucleotide polymorphisms (SNPs) in PEAR1 were all non-significant (p ≥ 0.059). With similar adjustments, the incidence of hypertension (397 cases among 1532 participants were normotensive at baseline [25.9%]) was not related to the SNPs in PEAR1 (hazard ratios ≤ 1.09; p ≥ 0.09). CONCLUSION: Our study suggests that PEAR1 is not a hypertension susceptibility gene in humans.
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Olivi et al. (2014) conducted a cohort in Hypertension (n=1,973). Genetic variation in PEAR1 (nine single nucleotide polymorphisms) was evaluated on Incidence of hypertension (HR ≤ 1.09, p=≥ 0.09). Genetic variation in PEAR1 was not significantly associated with the incidence of hypertension over a median 10-year follow-up (hazard ratios ≤ 1.09; p ≥ 0.09).
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