Fig. 5

The life cycle of a single mitochondrion. a Dynamic changes in mitochondrial networks. Mitochondrial networks change continually, alternating between hyperfusion and fragmentation. This dynamic balance is modulated by various physiological and pathological stimuli, including ischemia–reperfusion, cell apoptosis, mitochondrial depolarization, mitochondrial uncoupling, respiratory induction, starvation, stress, Ca²⁺ overload, and toxin accumulation. Hyperfused networks are associated with increased ATP production and reduced ROS generation. b Mitochondrial biogenesis occurs through symmetric division and is influenced by the cellular energy status, indicated by the NAD⁺/NADH ratio, AMP/ATP ratio, and levels of acetyl-CoA, ROS, Ca²⁺, and mitophagy activity. c Clearance of damaged mitochondria through proteases, proteasomes, transferosomes, MDVs, or mitochondrial fusion, followed by mitophagy as the final defense to maintain mitochondrial homeostasis. d Mitochondrial dynamic localization involves anterograde transport primarily mediated by Kinesin, retrograde transport mainly dependent on Dynein, and mitochondrial anchoring through SNPH and ER-mito contacts. e Mitophagy, including Ub-dependent mitophagy, receptor-dependent mitophagy, and receptor-independent mitophagy, followed by fusion with lysosomes to form autolysosomes