Inhibition of Sat1 alleviates myocardial ischemia-reperfusion injury through regulation of ferroptosis via MAPK/ERK pathway.

ABSTRACT:

Introduction

Myocardial ischemia-reperfusion injury (MIRI) is a prevalent complication in patients with myocardial infarction. The pathological mechanism of MIRI remains elusive. Ferroptosis plays a critical role in MIRI. This study aimed to investigate the role of spermidine/spermine N1-acetyltransferase 1 (Sat1) in MIRI by regulation of ferroptosis.

Methods

Rats and H9C2 cells were used to perform MIRI model. The extent of myocardial damage and associated pathological changes were evaluated. Protein expression was detected by western blot. Then we observed the mitochondrial morphology and measured cell viability and damage. The levels of lipid peroxide and glutathione were measured, and lipid reactive oxygen species (ROS) was quantified. Differentially expressed genes (DEG

SUBMITTER: Liu Z 

PROVIDER: S-EPMC11599858 | biostudies-literature | 2024

REPOSITORIES: biostudies-literature