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. 2014 Nov 25;308(3):H183–H192. doi: 10.1152/ajpheart.00708.2014

Fig. 3.

Fig. 3.

Induction of autophagy by damaged mitochondria. A: BH3-only proteins directly induce autophagy by disrupting the BCL-2/BECLIN1 complex to release BECLIN1. The BECLIN1/VPS34/VPS15 complex can then induce autophagy. B: damaged mitochondria produce less ATP production, which activates the energy sensor AMPK. AMPK then activates Unc-51-like kinase (ULK)1, which activates the BECLIN1/VPS34/VPS15 complex. C: damaged mitochondria produce reactive oxygen species (ROS) that inhibit mammalian target of rapamycin (mTOR). Inhibition of mTOR leads to activation of autophagy. D: opening of the mitochondrial permeability transition pore (mPTP) results in influx of solutes and water into the mitochondrial matrix, which leads to disruption of the proton gradient and oxidative phosphorylation. It also causes depolarization and mitochondrial swelling that can activate autophagy.