Fig. 1

MMA accumulation aggravates myocardial injury. In vitro, AC16 cells were treated with MMA (17.5 mM) for 3 h and employed for further analyses. In vivo, mice were assigned to the sham operation or myocardial ischemia–reperfusion (I/R) injury group. MMA (400 mg/kg/d) was administered seven days before sham and I/R surgery. a MMA level of patients was detected by ultra-performance liquid chromatography-quadrupole-electrostatic field orbitrap (UHPLC-Q-Orbitrap) (n = 15 in control group; n = 50 in AMI before PCI/AMI after PCI group). b Morphology was evaluated by light microscopy after AC16 cells were treated with MMA (Scale bar: 50 μm). c AC16 cells were treated with/without MMA in Normoxia or hypoxia-reoxygenation (H/R) condition. Cell viability was detected by 3-(4,5-dimthyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazoliumbromide (MTT) assay (n = 3–6/group). d Representative TEM images of AC16 cells treated with/without MMA. Yellow arrows indicate mitochondria (Scale bar: 20 μm). e Representative images of heart sections with TTC/Evans staining (Scale bar: 2 mm). The area of AAR was marked with yellow dotted line. f, g Ratios of area at risk (AAR) to left ventricular (LV) area and infarct area to AAR are shown (n = 3/group). h, i Representative photomicrographs and averaged data of TdT-mediated dUTP nick end labeling (TUNEL) positive cells (n = 4/group) (Scale bar: 100 μm). j Cardiac damage was indicated as CK-MB assay (n = 4/group). k Representative images of M-mode echocardiograms. l, m Quantitative analysis of ejection fraction (EF) and fractional shortening (FS) echocardiography (n = 3/group). Data are expressed as the mean ± standard deviation. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001 and n.s, not significant