NaV1.5 autoantibodies in Brugada syndrome: pathogenetic implications.

ABSTRACT:

Background and aims

Patients suffering from Brugada syndrome (BrS) are predisposed to life-threatening cardiac arrhythmias. Diagnosis is challenging due to the elusive electrocardiographic (ECG) signature that often requires unconventional ECG lead placement and drug challenges to be detected. Although NaV1.5 sodium channel dysfunction is a recognized pathophysiological mechanism in BrS, only 25% of patients have detectable SCN5A variants. Given the emerging role of autoimmunity in cardiac ion channel function, this study explores the presence and potential impact of anti-NaV1.5 autoantibodies in BrS patients.

Methods

Using engineered HEK293A cells expressing recombinant NaV1.5 protein, plasma from 50 BrS patients and 50 controls was screened for anti-NaV1.5 autoantibodies v

SUBMITTER: Tarantino A 

PROVIDER: S-EPMC11491155 | biostudies-literature | 2024 Oct

REPOSITORIES: biostudies-literature