Fig 2: Pearson correlation coefficient analysis of the relationship between the expression levels of miR-146b and miR-155, and concentrations of the parameters related with myocarditis in Treg cells. (A) The relationship between the expression levels of miR-146b and concentration of CK-MB. (B) The relationship between the expression levels of miR-146b and concentration of cTnI. (C) The relationship between the expression levels of miR-146b and concentration of GrB. (D) The relationship between the expression levels of miR-146b and concentration of sFasL. (E) The relationship between the expression levels of miR-146b and concentration of caspase-3. (F) The relationship between the expression levels of miR-155 and concentration of CK-MB. (G) The relationship between the expression levels of miR-155 and concentration of cTnI. (H) The relationship between the expression levels of miR-155 and concentration of GrB. (I) The relationship between the expression levels of miR-155 and concentration of sFasL. (J) The relationship between the expression levels of miR-155 and concentration of caspase-3. There is a strong positive relation between two variables if rho falls within from 0.5 to 1. The levels of CK-MB, cTnI, GrB, and sFasL were positively associated with the levels of miR-146b and miR-155.

Fig 3: Expression levels of miR-133a and endothelial injury markers (vWF, H-FABP and cTnI) in a rat model of acute myocardial infarction. (A) Quantification of the expression levels of miR-133a in model rats, as determined by RT-qPCR. Expression levels of (B) vWF, (C) H-FABP and (D) cTnI in model rats, as determined by ELISA. Data are presented as the mean ± standard deviation. *P<0.05 vs. the Con group; #P<0.05 vs. the Model group; &P<0.05 vs. the Mimic group. Con: Control group, rats that underwent the sham operation were injected with a vector; Model: Model group, rats in the AMI model group were injected with NC; mimic, miR-133a mimic group, rats in the AMI model group were injected with a miR-133a mimic; inhibitor, miR-133a inhibitor group, rats in the AMI model group were injected with a miR-133a inhibitor; cTnI, cardiac troponin I; H-FABP, heart-type fatty acid-binding protein; miR-133a, microRNA-133a; vWF, Von Willebrand factor.

Fig 4: Expression levels of miR-133a and endothelial injury markers (vWF, H-FABP and cTnI) in patients with or without AMI. The expression levels of miR-133a, and vWF, H-FABP and cTnI, were detected in patients using reverse transcription-quantitative polymerase chain reaction and ELISA, respectively. AMI patients, patients with AMI following radical surgery for gastric cancer; Control patients, patients without AMI following radical surgery for gastric cancer. Data are presented as the mean ± standard deviation. *P<0.05 vs. the Control patients. AMI, acute myocardial infarction; cTnI, cardiac troponin I; H-FABP, heart-type fatty acid-binding protein; miR-133a, microRNA-133a; vWF, Von Willebrand factor.

Fig 5: Measurement of the serum levels of GPX4, SIRT1, markers of cardiac injury, and markers of the oxidative stress responses in the clinical samples and rat SIC models. Serum levels of (A) GPX-4 and SIRT1, (B) CK-MB and cTnI and (C) TNF-α and IL-6 in SIC patients and healthy donors. (D) Correlation between GPX4, SIRT1, CK-MB, and cTnI in the 20 SIC patients. Serum levels of (E) GPX-4 and SIRT1, and (F) of cardiac injury markers in the rat model of SIC. (G) Inflammatory cell infiltration in the rat cardiac tissues was assessed using hematoxylin and eosin staining. *P<0.05, **P<0.01, ***P<0.001. GPX4, glutathione peroxidase 4; SIC, Sepsis-induced cardiomyopathy.