Stimulation of the mitochondrial calcium uniporter mitigates chronic heart failure-associated ventricular arrhythmia in mice.

ABSTRACT:

Background

An aberrant increase in the diastolic calcium concentration ([Ca²⁺]_i) level is a hallmark of heart failure (HF) and the cause of delayed afterdepolarization and ventricular arrhythmia (VA). Although mitochondria play a role in regulating [Ca²⁺]_i, whether they can compensate for the [Ca²⁺]_i abnormality in ventricular myocytes is unknown.

Objective

The purpose of this study was to investigate whether enhanced Ca²⁺ uptake of mitochondria may compensate for an abnormal increase in the [Ca²⁺]_i of ventricular myocytes in HF to effectively mitigate VA.

Methods

We used a HF mouse model in which myocardial infarction was induced by permanent left anterior descending co

SUBMITTER: Hagiwara H 

PROVIDER: S-EPMC10746330 | biostudies-literature | 2022 Oct

REPOSITORIES: biostudies-literature