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Fig. 2 | The Journal of Physiological Sciences

Fig. 2

From: Mst1 promotes cardiac ischemia–reperfusion injury by inhibiting the ERK-CREB pathway and repressing FUNDC1-mediated mitophagy

Fig. 2

Mst1 deletion improves cardiac function in the context of cardiac I/R injury. a–c Cardiac function was measured via echocardiography. FS fractional shortening, LVDd left ventricular diastolic dimension, LVEF left ventricular ejection fraction. d–f After cardiac I/R injury, blood was collected and the concentrations of cardiac damage markers were detected via ELISA. LDH lactate dehydrogenase; CK-MB: creatine kinase-MB. g–l The contractile properties of cardiomyocytes in WT mice and Mst1-KO mice in the context of IR injury. +dL/dt is the maximal velocity of shortening. −dL/dt is the maximal velocity of relengthening. TPS is the time to peak shortening. TR90 is the time to 90% relengthening. m–o Cardiomyocyte calcium mapping via the Fluo-2 probe. Representative tracings of F340/F380 fluorescence ratio. The calcium transient baseline and the amplitude of calcium transients were measured. Data are presented as the mean ± SEM (n = 6, for each group). I/R injury ischemia–reperfusion injury. *P < 0.05

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