Figure 6.

Hsc70 knock‐down induced mitochondria‐LDs disassociation and lipid accumulation in hearts of NTG and Mfn2^TG mice. A) Mice were intra‐myocardial injected with control adeno‐associated virus 9 (AAV‐9) or recombined AAV‐9 encoding Hsc70 shRNA and then subjected to10 weeks’ CD or HFD feeding. LDs are labeled as green while mitochondria are labeled as red. Scale bars, 1 µm. B) Intra‐myocardial LD number were calculated to assess lipid accumulation in myocardium (Mean± SEM, n = 15 images from 8 mice each group, **P<0.01). C) Percentage of LDs contact with mitochondria (Mean± SEM, n = 15 images from 8 mice each group, **P<0.01). D) Mean LD‐mitochondria contact length were measured to reflect LD‐mitochondria tethering in myocardium. (Mean± SEM, n = 15 images from 8 mice each group, **P<0.01). E–I) Echocardiographic assessment were performed on NTG and Mfn2^TG mice treated as indicated. n = 8 mice per group. E) Representative images of M‐mode echocardiography (above) and representative Doppler flow measurement of mitral inflow (below). F–I) left ventricle ejection fraction (LVEF), left ventricle fractional shortening (LVFS), E/A ratio and isovolumic relaxation time (IVRT). (Mean± SEM, **P<0.01). CD, chow diet; HFD, high‐fat diet; LD, lipid droplet.