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Proteomics study of right atrium in patients with atrial fibrillation after coronary artery bypass grafting

ABSTRACT: We performed 4D-labelfree quantitative proteomics analysis of right atrial appendage tissues from 5 patients with atrial fibrillation (AF) and 5 patients with sinus rhythm (SR) after CABG. A total of 2179,559 spectrums and 48,047 peptides were detected by mass spectrometry. Further, we identified 5002 proteins, of which the number of comparable proteins was 4166. Finally, compared with SR group, 108 proteins were up-regulated and 25 proteins were down-regulated in AF group (AF/SR > 1.5, P < 0.05).

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Heart

SUBMITTER: Hai-Tao Hou

LAB HEAD: Hou HT

PROVIDER: PXD059685 | Pride | 2025-08-11

REPOSITORIES: Pride

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			Action	DRS
	XA02141B2LQ_AF_1_Slot1-35_1_5001.d.zip	Other
	XA02141B2LQ_AF_2_Slot1-36_1_5002.d.zip	Other
	XA02141B2LQ_AF_3_Slot1-37_1_5003.d.zip	Other
	XA02141B2LQ_AF_4_Slot1-38_1_5005.d.zip	Other
	XA02141B2LQ_AF_5_Slot1-39_1_5006.d.zip	Other

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Publications

Atlas of lysine propionylation of human right atrium and ALDH6A1-NADH pathway in new-onset atrial fibrillation after coronary surgery.

Zhang Yi Y Chen Huan-Xin HX Hou Hai-Tao HT Liu Ying-Qi YQ Chen Zhuo Z Yang Qin Q He Guo-Wei GW

Communications biology 20250604 1

Lysine propionylation modification (Kpr) plays an important role in the pathogenesis of several cardiovascular diseases, but the role of Kpr in postoperative atrial fibrillation (POAF) is unclear. Here, we established an atlas of proteomics and propionylation proteomics in the atrial appendage tissues from 28 CABG patients, exploring the role of Kpr proteins in the occurrence of POAF. The Kpr of ALDH6A1 was most significantly increased on Lys113 (2.25 folds). The activity of ALDH6A1 increased du ...[more]

PMID: 40467924

Similar Datasets

Atlas of lysine propionylation in the human right atrium reveals ALDH6A1-NADH pathway involved in the new-onset atrial fibrillation in aging after coronary artery bypass grafting

Project description:Lysine propionylation modification (Kpr) plays an important role in the pathogenesis of several cardiovascular diseases, but the role of Kpr in postoperative atrial fibrillation (POAF) is unclear. Here, we established an atlas of proteomics and propionylation proteomics in the atrial appendage tissues from 28 aging CABG patients, exploring the role of Kpr proteins in the occurrence of POAF. The Kpr of ALDH6A1 was most significantly increased on Lys113 (2.25 folds). The activity of ALDH6A1 increased due to higher binding energy of propionylated ALDH6A1 and NAD+, causing an increase in NADH levels in cells and triggering abnormal energy metabolism. Furthermore, the increase in NADH levels triggered the accumulation of reactive oxygen species, which may cause oxidative stress and cardiac electrical remodeling, resulting in the development of AF. This study reveals the important role of ALDH6A1-NADH pathway in POAF, and provides new insights for exploring the pathogenesis of POAF in CABG.

2025-08-11 | PXD059607 | Pride

Valvular heart disease and atrial fibrillation regulate microRNA expression profiles in left and right atria differently

Project description:Background: Chronic atrial fibrillation (AF) is a complication associated with the dilated atria of patients with valvular heart disease and contributes to worsened pathology. Methods and Results: Using microarray technology, we examined microRNA (miR) expression profiles in right and left atrial appendage tissue from valvular heart disease (VHD) patients. Right atrial appendage from patients undergoing coronary artery bypass grafting (CABG) and left atrial (LA) appendage from healthy hearts not used for transplant were used as controls. VHD induced different changes in miR expression in LA compared with right atria (RA). Fifty-two (52) miRs were altered by VHD in LA, compared with 5 in RA tissue. There was no detectable effect of chronic AF on miR expression in LA tissue, but miR expression in RA was strongly influenced by AF, with 47 miRs showing differential expression. LA volume correlated with miR expression changes in both LA and RA, but the affected miRs were different for the two atrial groups. Conclusions: VHD and AF influence miR expression patterns in LA and RA, but these are affected differently by disease progression and by the development of AF. These findings provide new insights into the progression of VHD. RA tissue is not a useful surrogate for LA in studies of mitral valve disease. 34 arrays from either the left or right atrium from patients with Valvular Heart Disease (VHD), patients undergoing coronary artery bypass grafting (CABG), or healthy controls. Arrays in this series were generated on V2 and V3 Agilent microRNA arrays and analysed in combination.

2011-12-21 | E-GEOD-28954 | biostudies-arrayexpress

Rac1-Induced Connective Tissue Growth Factor regulates Connexin 43 and N-Cadherin Expression in Atrial Fibrillation

Project description:Objectives: We studied the signal transduction of atrial structural remodelling that contributes to the pathogenesis of atrial fibrillation (AF). Backround: Fibrosis is a hallmark of arrhythmogenic structural remodelling but the underlying molecular mechanisms are incompletely understood. Methods: We performed transcriptional profiling of left atrial myocardium (LA) from patients with AF and sinus rhythm (SR) and applied cultured primary cardiac cells and transgenic mice with overexpression of constitutively active V12Rac1 (RacET) who develop AF at old age to characterize mediators of the signal transduction of atrial remodeling. Results: LA from patients with AF showed a marked upregulation of connective tissue growth factor (CTGF) expression compared SR patients. This was associated with increased fibrosis, NADPH-oxidase-, Rac1- and RhoA activity, upregulation of N-cadherin and connexin 43 (Cx43) expression and increased angiotensin II tissue concentration. In neonatal rat cardiac myocytes and -fibroblasts, a specific small molecule inhibitor of Rac1 or simvastatin completely prevented the angiotensin II induced upregulation of CTGF, Cx43 and N-cadherin expression. Transfection with small-inhibiting CTGF RNA blocked Cx43 and N-cadherin expression. RacET mice showed upregulation of CTGF, Cx43 and N-cadherin protein expression. Inhibition of Rac1 by oral statin treatment prevented these effects, identifying Rac1 as a key regulator of CTGF in vivo. Conclusion: The data identify CTGF as an important mediator of atrial structural remodelling during AF. Angiotensin II activates CTGF via activation of Rac1 and NADPH oxidase, leading to upregulation of Cx43, N-cadherin and interstitial fibrosis and therefore contributing to the signal transduction of atrial structural remodelling. Array design study consists of 5 Atrial Fibrillation patients and matched 5 samples of patients in sinus rhythm (controls).

2010-02-21 | E-GEOD-14975 | biostudies-arrayexpress

Array-based genome-wide transcriptome analysis of the left atrial appendage for the difference between SR maintenance group and AF recurrence group

Project description:Atrial fibrillation (AF), which causes cardiogenic cerebral infarction, is the most common type of persistent arrhythmia, and its incidence increases with age. We performed a radial procedure using an RF ablation device to restore sinus rhythm (SR).

2021-08-01 | GSE176166 | GEO

Integrated Analysis of Dysregulated lncRNA and mRNA Expression profiles of myocardial sleevesof pulmonary veins in atrial fibrillation

Project description:Atrial fibrillation (AF) is currently the most prevalent arrhythmia worldwide.Recent clinical data implicate the additional contribution of non-coding RNAs in the pathogenesis of AFï¼which include microRNAs(miRNAs), endogenous small interfering RNAs, PIWIinteracting RNAs, and lncRNA. Notably, a growing number of lncRNAs have been implicated in disease etiology, although an association with AF has not been reported. In the present study, we conducted an integrated analysis of dysregulated lncRNA and mRNA expression profiles in myocardial sleevesof pulmonary veins between the patients who develop AF and the patients who were in normal sinus rhythm, which was performed using a second generation lncRNA microarrayï¼focusing specifically on the identification and characterization of lncRNAs and mRNA potentially involving in maintaining atrial fibrillation. We conducted an integrated analysis of myocardial sleeves of pulmonary veinsï¼PVsï¼from 12 patients (6 non-AF and 6AF) in our center, of which hypertension, diabetes, smoking and alcohol abuse were excluded, using a second generation lncRNA microarray

2016-01-16 | E-GEOD-76899 | biostudies-arrayexpress

Endothelial plasticity in atrial fibrosis by integrating single-cell sequencing and genetic lineage tracing

Project description:Background and aims: Atrial fibrosis represents a critical determinant in atrial fibrillation (AF) pathogenesis. Although endothelial dysfunction is a hallmark feature of AF, the precise mechanisms by which endothelial cells (ECs) contribute to atrial fibrosis remain incompletely understood. Methods: This study employed single-cell RNA sequencing (scRNA-seq) to analyze intercellular communication networks in atrial tissues from both sinus rhythm (SR) and AF patients. Cdh5-CreERT2;RFP mice were generated to track endothelial plasticity following transverse aortic constriction (TAC). Cell-cell interactions were investigated using isolated human primary atrial ECs and fibroblasts (FBs) in vitro. To elucidate the regulatory role of endothelial-derived TGF-β1 on FB function, endothelial-specific Tgf-β1 knockout (Tgf-β1ECKO) mice were generated. Results: scRNA-seq analysis identified ECs as predominant signal-sending cells with extensive FB connectivity in both SR and AF atrial tissues. During fibrosis progression, ECs displayed significant mesenchymal activation at the transcriptional level. However, immunofluorescence and high-content screening revealed minimal complete endothelial-to-FB transition. Cell-cell communication analysis and in vitro studies identified TGF-β1 as the key mediator through which mesenchymal-activated ECs (EndoMA) promoted FB proliferation and collagen production. Notably, endothelial-specific Tgf-β1 deletion attenuated TAC-induced atrial fibrosis and reduced AF susceptibility. Conclusions: Our findings demonstrate that EndoMA-derived TGF-β1 critically regulates FB function and drives atrial fibrosis progression. Targeting endothelial-specific pathways represents a promising therapeutic strategy for attenuating atrial fibrosis in AF pathogenesis.

2025-08-27 | GSE198204 | GEO

Rac1-Induced Connective Tissue Growth Factor regulates Connexin 43 and N-Cadherin Expression in Atrial Fibrillation

2010-02-11 | GSE14975 | GEO

Changes of ubiquitylated proteins in atrial fibrillation associated with heart valve disease: proteomics in human in left appendage tissue

Project description:Atrial fibrillation (AF) is the most common persistent arrhythmia that affect 1–2% of the general population. People with AF display an array of complications cardiogenic stroke and systemic embolism caused by hemodynamic instability and blood hypercoagulability in clinical practice. However, it’s still unclear whether and how ubiquitylated proteins react to AF in the left atrial appendage of patients with AF and valvular heart disease. This theory focuses on the changes of ubiquitylated proteins in atrial fibrillation associated with heart valve disease. We firstly widely analysis the proteins ubiquitination in patients with atrial fibrillation.

2021-12-24 | PXD030397 | Pride

Profiling of long non-coding RNAs associated with atrial fibrillation in patients with rheumatic heart valvular disease

Project description:To investigate the expression profiles of long non-coding RNAs (lncRNAs) in atrial fibrillation (AF), atrial tissues from 5 AF patients and 5 non-AF patients that were collected for lncRNA expression microarray analyses to explore the role of lncRNA in the pathogenesis of AF.rhythm (SR) patients with rheumatic heart valvular disease,we have employed

2018-01-03 | GSE108660 | GEO

Using integrative bioinformatics approaches and machine‑learning strategies to Identify potential signatures for atrial fibrillation

Project description:Atrial fibrillation (AF) is the most common tachyarrhythmia and seriously affects human health. Key targets of AF bioinformatics analysis can help to better understand the pathogenesis of AF and develop therapeutic targets. The left atrial appendage tissue of 20 patients with AF and 10 patients with sinus rhythm were collected for sequencing, and the expression data of the atrial tissue were obtained. Based on this, 2578 differentially expressed genes were obtained through differential analysis. Different express genes (DEGs) were functionally enriched on Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG), mainly focusing on neuroactive ligand-receptor interactions, neuronal cell body pathways, regulation of neurogenesis, and neuronal death，regulation of neuronal death, etc. Secondly, 14 significant module genes were obtained by analyzing the weighted gene co-expression network of DEGs. Next, LASSO and SVM analyzes were performed on the differential genes, and the results were in good agreement with the calibration curve of the nomogram model for predicting AF constructed by the weighted gene co-expression network key genes. The significant module genes obtained by the area under the ROC curve (AUC) analysis were analyzed. Through crossover, two key disease characteristic genes related to AF, HOXA2 and RND2, were screened out. RND2 was selected for further research, and qPCR verified the expression of RND2 in sinus rhythm patients and AF patients. Patients with sinus rhythm were significantly higher than those in AF patients. Our study shows that RND2 can be used as a new target for the diagnosis and treatment of AF.

2025-01-29 | GSE282504 | GEO