Fig. 1
Proteomics showed that S100a9 was the main mediator underlying the decrease of myocardial autophagic flux. A Flowcharts of the quantitative proteomics performed in the present study. B The principal component analysis (PCA) of proteins by proteomics. C Number of identified peptide segments and proteins in the database after filtering. D Volcano plot of the proteins in the myocardial tissues of mice. The red dots indicate upregulated proteins, and the blue dots indicate downregulated proteins. E Venn diagram of the statistically significant proteins and autophagy-related proteins. F S100a9 expression levels were analyzed via western blot. G Mouse myocardial tissue sections were stained via immunofluorescence to detect the expression of S100a9 in cardiomyocytes. Representative immunofluorescence images showing α-actinin (red), S100a9 (green), and DAPI (blue). H S100a9 expression levels were detected after β1-AA stimulation for 12, 24, 36, 48 h in H9c2 cells. I S100a9 expression levels were detected via immunofluorescence staining after β1-AA stimulation for 24 h in H9c2 cells. S100a9 was stained with FITC (scale bar, 50 µm). Results are presented as the mean ± SEM with n = 6 per group. *p < 0.05 vs. control, **p < 0.01 vs. control. DEPs indicate differentially expressed proteins