Cytochrome c (CYCS)

Cytochrome c is a small (~12 kDa), highly conserved heme protein located primarily within the mitochondrial intermembrane space[1]. It functions as an electron carrier between Complex III (cytochrome bc1 complex) and Complex IV (cytochrome oxidase) of the respiratory electron transport chain—an essential process for ATP synthesis during oxidative phosphorylation[1][4]. Structurally, it consists of about 104 amino acids with a covalently attached heme group coordinated by histidine and methionine residues[1]. Beyond energy metabolism, it plays a pivotal role in intrinsic apoptosis; upon cellular stress or damage leading to mitochondrial outer membrane permeabilization, cytochrome c is released into the cytosol where it helps form the apoptosome complex with Apaf‑1—triggering caspase activation and programmed cell death[1]. Its involvement extends to redox homeostasis and peroxidase activity under certain conditions. Dysregulation of these processes links cytochrome c to various diseases including cancer, neurodegeneration, cardiovascular disorders, and other pathologies associated with impaired apoptosis or oxidative stress responses[7].

Other names

cytochrome-ccyt-cCYCcytochrome c oxidase (note: "cytochrome c oxidase" is a distinct enzyme complex but sometimes confused in literature)mitochondrial cytochrome c

Drugs or agents that affect cytochrome c typically act by modulating its release from mitochondria to the cytosol during apoptosis. This can be achieved by influencing mitochondrial membrane permeability or targeting proteins involved in apoptotic regulation.