Table 4.

Cardiac ultrastructure in ischemia/reperfusion (I/R) and myocardial infarction (MI).

Animal models of I/R and MI	Ultrastructural changes	Quantitative TEM?	References
A rat model of MI	Myocardial fiber network is disrupted. Mitochondria became smaller and round. ↑ Mitochondrial and autophagosome numbers. ↑ LC3II/I ratio and ↓ Parkin protein level. ↓ autophagic flux.	No	Wu et al., 2016
A mouse model of MI	↑ Large vacuoles resemble autophagosomes at the border zone and smaller autophagosomes at the remote zone of the infarct at 1-week post-MI. By 3-week post-MI, more autophagosomes and lysosomes were present in the remote zone, and autophagosome size in the border zone was smaller. Rapamycin ↑ presence of autophagosomes and lysosome, whereas hearts from bafilomycin injected group remained free of these organelles.	No	Kanamori et al., 2011a
MI in GFP-LC3 transgenic mice, treated with starvation and/or bafilomycin	Time-dependent ↑ of autophagosomes and electron-dense bodies at both the infarct and border zones following MI from 30 min to 24 h. ↑ Cathepsin D at 30 min−24 h, whereas LC3II at 4–24 h and p62 at 24 h. Immune-TEM with a cathepsin D antibody and enzyme cytochemistry for acid phosphatase were used to confirm that the electron-dense bodies were in fact lysosomes. Starvation ↑ autophagosomes and bafilomycin ↑ electron-dense bodies.	No	Kanamori et al., 2011b
Post-MI treatment of resveratrol	↑ Autophagic vacuoles and lysosomes in post-MI hearts, which were further ↑ with resveratrol and associated with a reduction in adverse remodeling. ↑ Autophagic vacuoles and lysosomes by resveratrol and attenuated by adenosine monophosphate-activated protein kinase (AMPK) inhibitor compound C in neonatal cardiomyocytes in vitro. ↑ Electron-dense lysosomes without increase of autophagosomes by chloroquine.	No	Kanamori et al., 2013

Highlighted in bold are the subcellular structures observed by TEM.