Fig. 4: KDM1A overexpression alleviates CME-induced GSH imbalance in cardiomyocytes.

A KDM1A expression in cardiomyocytes stimulated with hypoxia for 12, 24, and 48 h was assessed using western blotting. Detailed P values see (A). B Western blotting analysis of KDM1A, GCLM, and GLS protein levels in cardiomyocytes after KDM1A overexpression. KDM1A-overexpressed cardiomyocytes were stimulated with hypoxia for 24 h. P = 0.0004 for KDM1A, P = 0.0069 for GCLM, and P = 0.0110 for GLS in H9c2 cells, and P = 0.0002 for KDM1A, P = 0.0061 for GCLM, and P = 0.0200 for GLS in NRVM cells. C The GSH/GSSG ratio was calculated. Detailed P values see (C). D ROS production was assessed using DCFH-DA staining. Detailed P values see (D). E Western blotting analysis of KDM1A, GCLM, and GLS protein levels. Detailed P values see (E). Data are presented as mean ± standard deviation (SD). n = 4 represents four independent biological repetitions, and each biological repetition contains three technological repetitions. In A, B, D, E, experiments were repeated independently at least 4 times with similar results. Representative images from one experiment are shown. Unpaired two-tailed Student’s t-test (for B) and one-way ANOVA followed by Tukey’s test for multiple group comparison (for A, C–E) were used to analyze data. Source data are provided as a Source data file. KDM1A lysine-specific histone demethylase 1A, GSH glutathione, CME coronary microembolization, GCLM glutamate-cysteine ligase modifier subunit, GLS glutaminase, GSSG oxidized glutathione, ROS reactive oxygen species.