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Serum apelin is associated with left ventricular hypertrophy in untreated hypertension patients
Lijun Ye1, Fenghua Ding2, Liang Zhang3
1Department of Critical Care Medicine, Affiliated Hospital of Guangdong Medical College, No. 57 Southern Renmin Avenue, 524023, Zhanjiang, Guangdong, China. 605364024@qq.com.
Insights
Lower serum apelin levels are linked to left ventricular hypertrophy (LVH) in hypertensive patients. Apelin may serve as a predictor for LVH and plays a role in cardiomyocyte adaptation to hypertrophic stimuli.
Area of Science:
- Cardiology
- Endocrinology
- Molecular Biology
Background:
- Apelin, an endogenous ligand for the APJ receptor, has known associations with cardiac remodeling.
- The impact of serum apelin levels on the prevalence of left ventricular hypertrophy (LVH) in hypertensive individuals remains unclear.
Purpose of the Study:
- To investigate the association between serum apelin levels and the presence of LVH in untreated hypertensive patients.
- To explore the direct effect of apelin on cardiac hypertrophy in vitro.
Main Methods:
- Echocardiography was used to determine LVH in 344 untreated hypertensive patients.
- Serum apelin levels were measured, and cardiomyocytes were cultured and transfected with the apelin gene to assess direct effects on hypertrophy.
Main Results:
- Hypertensive patients with LVH exhibited significantly lower serum apelin levels compared to those without LVH.
- Serum apelin levels demonstrated robustness in discriminating between patients with and without LVH.
- In vitro studies showed that apelin overexpression inhibited Ang II-induced increases in cardiomyocyte size and protein content.
Conclusions:
- Clinical data establish a link between apelin and LVH, suggesting serum apelin as a potential predictor for LVH prevalence in hypertensive patients.
- In vitro evidence indicates the involvement of the apelin pathway in cardiomyocyte adaptation to hypertrophic stimuli.
Background:
Apelin is an endogenous ligand for the G protein-coupled receptor APJ. The association between apelin and cardiac modeling has been reported. However, if serum apelin affect the left ventricular hypertrophy (LVH) prevalence in hypertensive patients remains unknown.
Methods:
We enrolled 344 untreated hypertensive patients. The presence of LVH was determined by echocardiography. The blood was drawn from these patients and serum apelin level was detected. To study the direct effect of apelin on cardiac hypertrophy, cardiomyocytes were cultured and were transfected with apelin gene. Morphometric analysis and measurement of protein contain per cell were then performed.
Results:
We observed a significantly lower serum apelin level in hypertensive patients with LVH compared with those without LVH. Receiver operating characteristic analyses shows that serum apelin level is robust in discriminating patients with LVH from those without. Our in vitro study showed that cellular protein content and cellular size was increased by Ang II treatment, which can be markedly inhibited by the apelin over-expression in cultured cardiomyocytes.
Conclusion:
Our clinical date established a link between apelin and LVH, suggesting serum apelin may be used as a predicator for LVH prevalence in hypertensive patients. The direct evidence in vitro suggest apelin pathway is involved in the cardiomyocyte adaption to hypertrophic stimuli.
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