MARK2 and myocardial infarction: 2007), which likely occurred through the destroying of a large fraction of organelles (Zhu et al. 2007). Moreover, the suppression of autophagy could reduce MI sizes (Wang et al. 2015). Therefore, the role of autophagy in MI remains controversial. AMP-activated protein kinase (AMPK), a serine-threonine kinase, is important for maintaining energy homeostasis during cellular stress. AMPK activation can inhibit rapamycin (mTOR) via the mammalian target and, thus, triggers autophagy. AMPK-mTOR signalling plays a crucial role in cardiac function post-MI (Qi and Young 2015).