Serum apelin is associated with left ventricular hypertrophy in untreated hypertension patients

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. We enrolled 344 untreated hyperten...

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Veröffentlicht in:Journal of translational medicine 2015-09, Vol.13 (1), p.290-290, Article 290
Hauptverfasser: Ye, Lijun, Ding, Fenghua, Zhang, Liang, Shen, Anna, Yao, Huaguo, Deng, Liehua, Ding, Yuanlin
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Sprache:eng
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Zusammenfassung: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. 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. 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. 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.
ISSN:1479-5876
1479-5876
DOI:10.1186/s12967-015-0635-5