Figure 2.

Schematic mechanisms of mitochondrial fusion, fission and mitophagy. Mitochondria cyclically shift between elongated (tubular) and fragmented state. The localization, as well as some interactions and modifications of the principal proteins involved in the two processes are shown. Once dephosphorylated, DRP1 (dynamin‐related protein 1) is recruited to the outer membrane by FIS1 (fission protein 1). The oligomerization of DRP1 is followed by constriction of the membrane and mitochondrial fission. Following the fission event, the mitochondrion can either be transported, or enter in fusion again. The pro‐fusion proteins mitofusin 1 and 2 (MFN1/2) on the outer membrane and optic atrophy 1 (OPA1) on the inner membrane) oligomerize to induce fusion of the membranes. Defective mitochondrion accumulates PINK1 kinase (PTEN‐induced putative kinase 1), recruiting the E3 ubiquitin ligase parkin, which ubiquitylates mitochondrial proteins and triggers mitophagy. The potential effects of aging on mitochondrial dynamics are marked by *. CAMK1α; Ca²⁺/calmodulin‐dependent protein kinase Iα, PKA: protein kinase A