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. 2014 May 1;124(6):2410–2424. doi: 10.1172/JCI66339

Figure 1. Atrogin-1 KO mice develop an age-related cardiomyopathy.

Figure 1

(A) Hearts from 6-, 9-, and 16-month-old control and atrogin-1 KO mice. (B) Evaluation of the heart weight/body weight (HW/BW) ratio in 6-, 9-, and 16-month-old control (C) and atrogin-1 KO mice. Error bars indicate SEM (**P < 0.01; n = 6 hearts for each group). (C) Confocal immunofluorescence on ventricular cryosections from 6-, 9-, and 16-month-old control and atrogin-1 KO mice stained with an antibody against dystrophin. Images show details from the RV. Scale bar: 50 μm. The morphometric evaluation of RV cardiomyocyte cross-sectional area is also shown. Error bars indicate SEM (**P < 0.01; n = 6 hearts for each group). (D) Evaluation of LV cardiomyocyte area in 6-, 9-, and 16-month-old control and atrogin-1 KO mice. Error bars indicate SEM (**P < 0.01; n = 6 hearts for each group). (E) Confocal immunofluorescence on LV cryosections from aged control and atrogin-1 KO hearts stained with an antibody against dystrophin, showing the mixture of normal sized and hypertrophic cardiomyocytes. Scale bar: 50 μm. (F) Evaluation of cardiomyocyte size distribution in the LV of 16-month-old control and atrogin-1 KO hearts. (G) Western blotting on ventricular extracts from aged control and atrogin-1 KO hearts. (H and I) Confocal immunofluorescence analysis of ventricular cryosections from aged control and atrogin-1 KO mice stained with antibodies to (H) β-myosin heavy chain and (I) atrial natriuretic factor. Scale bar: 50 μm.