Mitochondria are dynamic organelles that need to maintain their morphology for the optimal production of ATP under different metabolic conditions and as part of a healthy network of mitochondria. Fission and fusion are two processes that are necessary for the maintenance of mitochondria morphology. Mitochondria fuse together via mitofusin 1 (MFN1) and MFN2 (outer membrane fusion) and the activation of dynamin-like 120 kDa (OPA1) (inner membrane fusion). Fusion can occur to maintain ATP production or to redistribute mitochondrial proteins. Fission can isolate depolarized mitochondrion that might not contribute to the healthy network of mitochondria. The activation of fission causes the oligomerization of dynamin 1-like protein (DRP1) on the mitochondrial outer membrane, where it is bound to receptors (namely mitochondrial fission 1 (FIS1) and mitochondrial fission factor (MFF)), forming a ring-like structure that mediates the separation of mitochondria. The network also isolates dysfunctional mitochondria for degradation by mitophagy via a well-studied PTEN-induced putative kinase 1 (PINK1)– PARKIN mechanism. Under adverse conditions such as hypoxia, however, mitochondria will be removed by a FUN14 domain-containing protein 1 (FUNDC1) or BCL2/adenovirus E1B 19 kDa protein-interacting protein 3 (BNIP3) and NIP3-like protein (NIX)-dependent mechanism of mitophagy. LC3, microtubule-associated protein 1 light chain 3; Ub, ubiquitin.