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Figure 4 Autophagy and ischaemia–reperfusion

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1 Figure 4 Autophagy and ischaemia–reperfusion
Figure 4 | Autophagy and ischaemia–reperfusion. Transverse view of the heart showing the ischaemic 'at risk' zone (grey) and the postreperfusion necrotic area (black). During ischaemia (blue shaded area), activation of autophagy is linked with ATP depletion, activation of 5′-AMP-activated kinase (AMPK) and glycogen synthase kinase (GSK)-3β, and inhibition of mechanistic target of rapamycin complex 1 (mTORC1). During reperfusion (pink shaded area), a surge in the production of reactive oxygen species (ROS) is associated with inhibited GSK-3β activity and ATP levels are at least partially restored. Question marks highlight areas of uncertainty requiring further investigation. Some data indicate that sustained mTORC1 inhibition and AMPK activation are linked with elevated autophagy during reperfusion. Delbridge, L. M. D. et al. (2017) Myocardial stress and autophagy: mechanisms and potential therapies Nat. Rev. Cardiol. doi: /nrcardio


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