Abstract
BackgroundCongestive heart failure (CHF) is a major cause of the development of progressive chronic kidney disease (CKD), while the mechanism is still unknown. LncRNA PVT1 contributes to kidney injury. This study aimed to explore the role of PVT1 in the development of CKD in CHF patients.MethodsExpression of PVT1 in plasma samples of CHF patients with and without CKD was determined by RT-qPCR. The diagnostic value of plasma PVT1 for CKD was evaluated by ROC curve analysis. The predictive value of PVT1 for the development of CKD in CHF patients was analyzed by a 2-year follow-up study. Changes in PVT1 expression in CKD patients during treatment were analyzed by RT-qPCR and reflected by heatmaps.ResultsPlasma PVT1 was downregulated in CHF and further downregulated in CHF patients complicated with progressive CKD. ROC curve analysis showed that plasma PVT1 levels could be used to distinguish CHF patients complicated with CKD from CHF patients without CKD and healthy controls. During a 2-year follow-up, patients with high CHF levels had a low incidence of progressive CKD among CHF patients. Moreover, with the treatment of progressive CKD, plasma PVT1 was upregulated.ConclusionsLncRNA-PVT1 downregulation may participate in the development of progressive CKD among patients with CHF.
Highlights
Congestive heart failure (CHF), known as heart failure, is a common clinical disorder reflected by reduced heart function and/or impaired heart structure [1]
Plasma PVT1 was downregulated in CHF and further downregulated in CHF + chronic kidney disease (CKD) PVT1 levels in plasma samples collected from the control group (n = 50), CHF group (n = 100), and CHF + CKD group (n = 50) were measured by RT-qPCR
Plasma PVT1 levels were significantly lower in CHF (1.65-fold) and CHF + CKD (2.22-fold) groups than in the control group (p < 0.01)
Summary
Congestive heart failure (CHF), known as heart failure, is a common clinical disorder reflected by reduced heart function and/or impaired heart structure [1]. The molecular mechanisms linking CHF and CKD are unclear, limiting the development of preventative and treatment approaches [7]. Without protein-coding capacity, lncRNAs participate in CHF and CKD mainly by regulating related gene expression [8–10]. LncRNAs may be promising targets to understand the mechanism that mediates CKD development in CHF. The function of most lncRNAs in CDK and CHF remains unclear. Our preliminary microarray analyses revealed altered PVT1 expression in both CHF patients with and without CKD. Our study was performed to explore the potential involvement of PVT1 in the development of CKD in CHF. Congestive heart failure (CHF) is a major cause of the development of progressive chronic kidney disease (CKD), while the mechanism is still unknown. This study aimed to explore the role of PVT1 in the development of CKD in CHF patients
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