Salidroside protects against myocardial infarction via activating MIF-mediated mitochondrial quality control.

ABSTRACT:

Background

Salidroside is a potential therapeutic agent for myocardial infarction (MI), exerting therapeutic effects on macrophage migration inhibitory factor (MIF)-regulated mitochondrial quality control. Our aim was to explore the mechanism through which the MIF pathway regulates salidroside-mediated resistance to hypoxia-induced cardiomyocyte apoptosis.

Methods

Ligation surgery of the left anterior descending branch of the coronary artery was employed to establish a myocardial infarction mouse model. Salidroside at low and high doses was administered to the mice for 4 weeks after the surgery. Cardiac function was evaluated via echocardiography. Morphological changes, apoptosis, and mitochondrial damage in the myocardium were examined. For the cell experiments, cardiomyocy

SUBMITTER: You B 

PROVIDER: S-EPMC11869418 | biostudies-literature | 2025 Feb

REPOSITORIES: biostudies-literature