Lysosomal Ca²⁺ Release Through TRPML1 Governs Ventricular Arrhythmia After Myocardial Infarction.

ABSTRACT:

Background

In nonischemic cardiomyopathy, mitochondrial Ca²⁺ handling is involved in arrhythmogenesis by modulating diastolic sarcoplasmic reticulum (SR) Ca²⁺ release. Recently, it has been reported that lysosomal Ca²⁺ release can trigger an SR Ca²⁺ release. We investigated whether lysosomal Ca²⁺ flux through the TRPML1 (transient receptor potential mucolipin 1) channel could contribute to ischemic cardiomyopathy-related arrhythmia by causing diastolic SR Ca²⁺ release.

Methods

Ischemic cardiomyopathy was induced in wild-type C57BL/6J and TRPML1 heterozygous knockdown (TRPML1±) mice by ligating the left anterior descending coronary artery. Mice were studied at 3 weeks after myocardial infarction (MI).

Result

SUBMITTER: Xie A 

PROVIDER: S-EPMC12629118 | biostudies-literature | 2025 Nov

REPOSITORIES: biostudies-literature