# Comprehensive lnc-RNAs expression profiles in uremic cardiomyopathy before and after renal transplantation

## TL;DR

This study identifies lncRNA expression changes in uremic cardiomyopathy patients before and after kidney transplantation, revealing potential therapeutic targets.

## Contribution

The study provides novel insights into lncRNA expression patterns and their regulatory roles in UCM pathogenesis and recovery after renal transplantation.

## Key findings

- 769 dysregulated lncRNAs were identified in UCM patients before and after kidney transplantation.
- Lnc-LINC02194, lnc-MYOSLID-AS1, and lnc-LINC01229 showed significant expression changes validated by RT-qPCR.
- p53 and FoxO signaling pathways were implicated in UCM pathogenesis through lncRNA-mRNA interaction networks.

## Abstract

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.

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.

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.

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).

LncRNAs show significant correlation with UCM progression before and after renal transplantation. Lnc-LINC02194 may represent a candidate therapeutic target for UCM.