Differential Genes Analysis and Validation of Disulfideptosis in Rat Myocardial Ischemia-Reperfusion Injury Model.

Abstract

Myocardial ischemia-reperfusion injury (MIRI) is an additional injury that occurs during the process of restoring heart tissue blood flow after ischemia-induced injury. MIRI seriously affects the efficacy and short-term and long-term prognosis of reperfusion after myocardial infarction. At present, the mechanism of MIRI is not fully clear. Disulfideptosis is a novel mode of cell death, and the relationship between MIRI and disulfideptosis-related genes (DRGs) expression is still unclear. Firstly, this study explores the differentially expressed genes associated with disulfideptosis in MIRI through bioinformatics analysis. Secondly, by constructing a rat model of MIRI, DRGs were further detected. This study identified 12 related genes, including Myh9, SLC7A11, SLC3A2, Myh7b, ACTB, FLNB, Actn1, Actn4, Flnc, Dbn1 and Pdlim1. Myocardial tissue of rats with MIRI shows obvious pathological damage and apoptosis events. The results of immunohistochemistry indicated that MIRI stimulation increased the expression of GLUT1 protein in myocardial tissue but restricted the expression of F-actin protein. In addition, significant differences in the expression of three proteins were validated using external datasets and MIRI rat models. This study demonstrated that DRGs had significant predictive value in MIRI, providing new prospects for exploring biomarkers and potential therapeutic targets of MIRI.