Mitochondrial electron transport chain (ETC) and inner mitochondrial membrane redox system (ETC)

The mitochondrial electron transport chain (ETC) and inner mitochondrial membrane redox systems consist of a series of multi-subunit protein complexes (Complex I through IV) and mobile electron carriers like ubiquinone and cytochrome c (StatPearls: NBK526004). These systems facilitate the transfer of electrons from electron donors, such as NADH and FADH2, to a final electron acceptor, typically molecular oxygen, while simultaneously pumping protons across the inner mitochondrial membrane to create an electrochemical gradient. This gradient is subsequently utilized by ATP synthase (Complex V) to generate ATP, the primary energy currency of the cell (UniProt: Q02252). Beyond energy production, the ETC is a major site of reactive oxygen species (ROS) generation and plays a central role in initiating apoptosis through the release of cytochrome c (PubMed: 28844165). Dysfunction in these redox systems is a hallmark of various conditions, including primary mitochondrial diseases, neurodegeneration, and metabolic disorders (PubMed: 11017181). Therapeutic strategies targeting the ETC range from the use of inhibitors like metformin for metabolic control to the development of mitocans for cancer therapy, though such interventions must carefully balance efficacy with the risk of systemic mitochondrial toxicity (PubChem: CID 4091; PubMed: 24123360).

Other names

Respiratory chainOxidative phosphorylation systemOXPHOSMitochondrial respiratory chainInner mitochondrial membrane redox system

Inhibition of electron transfer between complexes, uncoupling of the proton gradient from ATP synthesis, and modulation of reactive oxygen species (ROS) generation (StatPearls: NBK526004; PubMed: 28844165).