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. Author manuscript; available in PMC: 2013 Oct 1.
Published in final edited form as: Kidney Int. 2013 Jan 16;83(4):568–581. doi: 10.1038/ki.2012.441

Figure 4. Mechanisms of mitochondrial fragmentation in cell death.

Figure 4

Upon cellular stress, Drp1 is activated and translocates to mitochondria to initiate mitochondrial fission by form a spiral constriction ring. Meanwhile, Bak is activated resulting in a shift of binding to Mfn1 and arrest of mitochondrial fusion. Together, the activation of mitochondrial fission and the arrest of mitochondrial fusion result in mitochondrial fragmentation. Fragmented mitochondria are sensitized to Bax insertion and oligomerization to induce the formation of pathological pores, i.e. MOMP, to trigger cell death. Drp1 is regulated by multiple post-translational modifications that may be induced by the increases of intracellular Ca2+ and ROS. In addition, Ca2+ and ROS can trigger MPT to induce MOMP or, directly, necrosis. As a cytoprotective mechanism, autophagy may remove fragmented mitochondria via mitophagy to suppress cell death.