Key result
Brugada Syndrome patients exhibited a significant increase in exosomal CNP mRNA expression and selective downregulation of miR-138-5p compared with healthy controls.
Why the study?
Atrial fibrillation is frequently observed in Brugada syndrome, but the roles of exosomal CNP and related microRNAs have not been investigated.
Do patients with Brugada Syndrome have altered exosomal CNP mRNA and CNP-related miRNA expression compared to healthy controls?
Case-Control
Do patients with Brugada Syndrome have altered exosomal CNP mRNA and CNP-related miRNA expression compared to healthy controls?
Exosomal profiling reveals increased CNP mRNA and downregulated miR-138-5p in Brugada Syndrome patients, suggesting a shared molecular substrate between atrial and ventricular arrhythmias.
Exosomal CNP mRNA upregulation with miR-138-5p downregulation may reflect shared arrhythmogenic pathways in Brugada syndrome; hypothesis-generating and requires prospective validation.
Background: Brugada Syndrome (BrS) is a cardiac arrhythmia associated with an increased risk of ventricular arrhythmias and sudden cardiac arrest. Although the arrhythmic substrate is traditionally localized to the ventricles, atrial fibrillation (AF) is frequently observed, suggesting a shared molecular substrate between atrial and ventricular arrhythmias. C-type natriuretic peptide (CNP) and related microRNAs (miRNAs) modulate atrial and ventricular physiology, but their roles in exosomes in BrS have not been investigated. Objectives: To investigate alterations in CNP mRNA expression and changes in the expression of selected CNP-associated miRNAs implicated in AF, both analyzed in exosomes isolated from individuals with BrS and from healthy controls. Methods: Exosomes were isolated from the plasma of BrS patients without a history of overt AF and from healthy controls. In silico analyses identified CNP-targeting miRNAs implicated in AF. Exosomal CNP and CNP-related miRNAs were analyzed using Droplet Digital PCR. Results: BrS patients exhibited a significant increase in exosomal CNP mRNA expression levels compared with controls. MiR-138-5p was selectively downregulated, whereas other AF-related CNP-targeting miRNAs (miR-4443, miR-206, miR-142-5p, miR-223-5p) showed comparable levels between groups. A positive correlation between exosomal CNP and miR-223-5p and miR-4443 suggests shared regulatory pathways. Conclusions: these findings indicate that exosomal profiling may provide a more sensitive approach than conventional circulating measurements to detect molecular remodeling in BrS. The observed alterations highlight a potential shared molecular substrate between atrial and ventricular arrhythmias and may inform future studies aimed at refining diagnostics and developing targeted therapeutic strategies.
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Cabiati et al. (2026) conducted a case-control in Brugada Syndrome. Brugada Syndrome vs. Healthy controls was evaluated on Exosomal CNP mRNA expression and CNP-associated miRNA levels. Brugada Syndrome patients exhibited a significant increase in exosomal CNP mRNA expression and selective downregulation of miR-138-5p compared with healthy controls.
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