Fig. 2: Genetic deletion of HIP-55 increases cardiomyocyte injury after MI.
From: Adaptor protein HIP-55-mediated signalosome protects against ferroptosis in myocardial infarction
A Genotyping of wildtype (WT) and HIP-55 knockout (HIP-55−/−) mice. B Western blot analysis of HIP-55 expression in the heart tissues of WT and HIP-55−/− mice. C Deletion of HIP-55 promoted myocardial infarction size. Representative Alcian blue-TTC staining (left) and quantitative analysis (right) for area at risk (AAR) and infarct size in hearts from the WT and HIP-55−/− mice post-MI. WT, n = 8; HIP-55−/−, n = 7. D HIP-55 deficiency significantly increased cardiac hypertrophy after MI. The ratio of heart weight to tibial length (HW/TL) in WT and HIP-55−/− mice after MI. n = 6–8. E Deletion of HIP-55 promoted MI-induced cardiac dysfunction. Representative M-mode echocardiographic photographs (left) and cardiac contractile function (right) quantified by echocardiographic analysis of ejection fraction (EF) and fractional shortening (FS) in WT and HIP-55−/− mice at day 7 after MI. n = 5–7. *P < 0.05, **P < 0.01. All error bars represent mean ± SEM.
