Ontology highlight
ABSTRACT: Background
Doxorubicin (DOX), a commonly used anticancer agent, can result in cardiac dysfunction, presenting a significant clinical challenge. DOX has been shown to induces Ca2+ leakage via the ryanodine receptor 2 (RYR2) of the sarcoplasmic reticulum, increasing Ca2+ levels in the cytoplasm.Objectives
This study investigated whether stabilizing RYR2 could suppress DOX-induced cardiomyopathy (DIC) and identified the optimal duration of dantrolene treatment as a pharmacological method.Methods
We investigated the effects of RYR2 stabilization on DOX cardiotoxicity using in vivo and in vitro experiments.Results
DOX administration caused calmodulin dissociation, marked Ca2+ leakage from RYR2, and increased oxidative stress in is
SUBMITTER: Nakamura Y
PROVIDER: S-EPMC11782101 | biostudies-literature | 2025 Jan
REPOSITORIES: biostudies-literature