C-Src Is Responsible for Mitochondria-Mediated Arrhythmic Risk in Ischemic Cardiomyopathy.

ABSTRACT:

Background

Increased mitochondrial Ca²⁺ uptake has been implicated in the QT prolongation and lethal arrhythmias associated with nonischemic cardiomyopathy. We attempted to define the role of mitochondria in ischemic arrhythmic risk and to identify upstream regulators.

Methods

Myocardial infarction (MI) was induced in wild-type FVB/NJ mice by ligation of the left anterior descending coronary artery. Western blot, immunoprecipitation, ECG telemetry, and patch-clamp techniques were used.

Results

After MI, c-Src (proto-oncogene tyrosine-protein kinase Src) and its active form (phosphorylated Src, p-Src) were increased. The activation of c-Src was associated with increased diastolic Ca²⁺ sparks, action potential duration prolongation, and arrhythmia

SUBMITTER: Xie A 

PROVIDER: S-EPMC11477858 | biostudies-literature | 2024 Oct

REPOSITORIES: biostudies-literature