FIGURE 5.

Overview of autophagy pathways following ICH. Oxidative stress, inflammation, and energy depletion after ICH may induce autophagy by activating adenosine monophosphate-activated protein kinase (AMPK) or inhibiting mammalian target of rapamycin (mTOR) and damaging mitochondria. During autophagy, light chain 3-II (LC3-II) in autophagosome and cathepsin D in lysosomes are increased. Excessive autophagy may be detrimental in the early stage of ICH, but maybe neuroprotective in the later stages through clearance of cellular debris.