Current medical research and opinion · 2026
Reduced plasma APJ levels and APLNR G212A polymorphism in Syrian patients with coronary artery disease.
СтатьяНаблюдательное исследованиеНазвание и аннотация: Перевод пока не подготовлен
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Abd-Alkareem Maisaa Hassan, Mohammed Shibli Hussam Eddin, Alquobaili Faizeh Ali
Аннотация
BACKGROUND: Coronary artery disease (CAD) remains a leading global cause of mortality. The apelin/apelin receptor (APJ) system has emerged as a novel pathway implicated in cardiovascular regulation and disease progression. This pioneering case-control study, the first conducted in a Syrian population, investigated the association of the apelin receptor G212A polymorphism and plasma APJ levels with CAD susceptibility.
METHODS: The participants comprised 108 CAD patients confirmed by angiography and 114 healthy controls. Plasma APJ levels were quantified via enzyme-linked immunosorbent assay (ELISA), and the apelin receptor G212A genotype and allele frequencies were determined using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). The study was registered on ClinicalTrials.gov (Identifier: NCT05562687).
RESULTS: Plasma APJ levels were significantly lower in CAD patients compared to controls (p < 0.005). Multivariable regression analysis further revealed that plasma APJ levels were independently associated with CAD and hypertension. While the heterozygous GA genotype and the A allele showed higher frequencies in CAD patients, no statistically significant association of the G212A polymorphism was observed between the patient and control groups (p > 0.05). Notably, the homozygous mutant AA genotype was not detected in any study participant.
CONCLUSION: Our findings indicate significantly reduced plasma APJ levels in Syrian CAD patients, suggesting a diminished protective role of the apelin/APJ system in disease pathophysiology. Despite observed trends, the apelin receptor G212A polymorphism was not significantly associated with CAD risk in this specific cohort. This highlights the potential of plasma APJ as a biomarker and underscores the importance of population-specific genetic studies.
METHODS: The participants comprised 108 CAD patients confirmed by angiography and 114 healthy controls. Plasma APJ levels were quantified via enzyme-linked immunosorbent assay (ELISA), and the apelin receptor G212A genotype and allele frequencies were determined using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). The study was registered on ClinicalTrials.gov (Identifier: NCT05562687).
RESULTS: Plasma APJ levels were significantly lower in CAD patients compared to controls (p < 0.005). Multivariable regression analysis further revealed that plasma APJ levels were independently associated with CAD and hypertension. While the heterozygous GA genotype and the A allele showed higher frequencies in CAD patients, no statistically significant association of the G212A polymorphism was observed between the patient and control groups (p > 0.05). Notably, the homozygous mutant AA genotype was not detected in any study participant.
CONCLUSION: Our findings indicate significantly reduced plasma APJ levels in Syrian CAD patients, suggesting a diminished protective role of the apelin/APJ system in disease pathophysiology. Despite observed trends, the apelin receptor G212A polymorphism was not significantly associated with CAD risk in this specific cohort. This highlights the potential of plasma APJ as a biomarker and underscores the importance of population-specific genetic studies.