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. Author manuscript; available in PMC: 2024 Mar 1.
Published in final edited form as: Nat Rev Mol Cell Biol. 2023 Jun 5;24(9):651–667. doi: 10.1038/s41580-023-00613-y

Fig. 4 ∣. Two types of actin induced by mitochondrial damage.

Fig. 4 ∣

Treatment with a number of mitochondrial inhibitors (CCCP, antimycin, rotenone, oligomycin, hypoxia, metformin) leads to rapid actin polymerization around the mitochondrion, which we refer to as acute damaged-induced actin (ADA). Appearance of ADA generally starts within 1–2 min of treatment and depolymerizes within 10 min of assembly. ADA has two effects: glycolytic stimulation and inhibition of inner mitochondrial membrane rearrangements (circularization). Mitochondrial circulation ensues after actin depolymerization. After approximately 1 h, a second round of actin polymerization occurs, which we refer to as prolonged damage-induced actin (PDA). PDA has three demonstrated effects that favour mitophagy: inhibition of fusion, even if the damaged mitochondrion repolarizes; dispersal of mitochondrial aggregates; and recruitment of core autophagy components.