Abstract

Background Chronic kidney disease (CKD) significantly contributes to increased cardiovascular morbidity and mortality. CKD-induced cardiac remodeling, clinically termed uremic cardiomyopathy (UCM), manifests as morphological and physiological alterations in the myocardium. While renal transplantation is known to mitigate uremia's effects on myocardial remodeling, improve cardiac function, and reverse damage, its underlying biological mechanism remains unclear. Exosomes mediate inter-organ communication, with their nucleic acid components serving as key regulatory molecules. Emerging evidence indicates long non-coding RNAs (lncRNAs) critically participate in cardiac disease mechanisms. Objective This study aimed to analyze the expression profile of blood exosome-derived lncRNAs in UCM patients before and after transplantation to explore lncRNA expression patterns, regulatory mechanisms, and identify key lncRNAs involved in UCM pathogenesis. Patients and methods Our study utilized high-throughput RNA sequencing to identify differentially expressed long non-coding RNAs (lncRNAs) in patients with uremic cardiomyopathy (UCM) before and after kidney transplantation. We analyzed the differential expression of lncRNAs from multiple perspectives, including expression profiles, lncRNA-mRNA interaction networks, and enriched GO and KEGG pathways, followed by validation through RT-qPCR. Results Gene sequencing revealed 769 dysregulated lncRNAs [440 downregulated, 329 upregulated; log2(fold change) > 2.0, p  < 0.05]. Computational biological analysis implicated p53 and FoxO signaling pathways in UCM pathogenesis. Differential lncRNA-mRNA interaction networks identified three potential UCM-associated genes: lnc-LOC105379080, lnc-LOC101927608, and lnc-LOC105369947. RT-qPCR validation confirmed significant upregulation of lnc-LINC02194 ( p  = 0.0003), and lnc-MYOSLID-AS1 ( p  = 0.0030), and significant downregulation of lnc-LINC01229 ( p  = 0.0052). Conclusion LncRNAs show s