Figure 1. Schematic diagram of RIRR and mitochondria-driven ROS propagation.

Oxidative phosphorylation occurring in the mitochondrial electron transport chain is an ATP producing mechanism. During this respiration process, ROS are also produced when high-energy electrons escape before they reach the final acceptor O₂. ROS induce a rapid depolarization of mitochondrial inner membrane potential and subsequent impairment of oxidative phosphorylation. Damaged mitochondria produce more ROS, especially the superoxide anion (O₂ ⁻) and hydrogen peroxide (H₂O₂), which potentiates RIRR and mitochondria-driven ROS propagation via activation of an inter-mitochondria signaling network. Therefore, loss of function in only a fraction of the mitochondria may eventually affect the viability of the whole cell through this positive feedback loop.