Abstract
BackgroundAtrial fibrillation (AF) is one of the most common arrhythmia encountered in the clinical practice. The estimated prevalence of AF in the general population is as high as 1–2%. In this study, we aimed to identify the molecular changes and mechanisms responsible for chronic atrial fibrillation in rheumatic heart disease (RHD).MethodsPatients with rheumatic heart diseases (N=162) were enrolled in this study and classified into chronic AF group and sinus rhythm (SR) group based on their clinical manifestation. The atrial tissue (N=62) and plasma (N=100) samples were collected from the patients undergoing valve replacement surgery. Multi‐omics Studies were fulfilled with RNA Sequencing (RNA‐seq), isobaric tags for relative and absolute quantification (iTRAQ) and gas chromatography‐mass spectrometer (GC‐MS). ELISA was used to validate the proteins.ResultsThe differential genes/proteins were identified in the tissue or in the plasma samples between RHD‐AF patients and RHD‐SR patients. Combined analysis of transcriptomics, proteomics, and metabolomics revealed that the PPAR signaling pathway plays an important role in AF. The expression of multiple proteins were associated with PPARα,β,γ in tissue samples. On the other hand, only PPARα downstream alternations were identified in the study of plasma samples (APO‐A1 and APO‐A2). These proteins may be potential biomarkers for the diagnosis and treatment of AF in the future.ConclusionsWe for the first time identified the differentially expressed genes/proteins and related metabolites from plasma and tissue in chronic AF patients. Our study suggests that AF may impair the energy metabolism in the heart by altering the PPAR pathway, thus presenting metabolic remodeling in the heart.Support or Funding InformationSupported by grants from the National Natural Science Foundation of China (81641017), Zhejiang Provincial Natural Science Foundation (LY15H020008), & Tianjin Binhai Key Platform for Creative Research Program (2012‐BK110004), Binhai New Area Health Bureau (2014BHKY010, 2012BWKZ008, 2016BWKY007, 2016BWKZ003).This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
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