Figure 1.

Overview of mitochondria tricarboxylic acid cycle (TCA) and electron transport chain (ETC). Coupling of TCA with the ETC is named oxidative phosphorylation (OxPhos) and is the main metabolic source of intracellular energy in the form of ATP. During the ETC, pooling of electrons (e⁻) inside the ETC proteinic complexes, for instance due to imbalances between electron feeding and ETC capacity, leads to release of reactive oxygen species (ROS). To protect the cell from the effects of this oxidative stress, mitochondrial existence is coupled with an intrinsic ability of the organelle to induce cellular death, when its function is compromised. Ca⁺² and/or other stimuli activate this intrinsic apoptotic pathway, which leads to increased mitochondrial outer membrane permeabilization. Release to the cytoplasm of the normal mitochondrial membrane-bound cytochrome c (Cyt c) activates a positive caspase regulatory cascade that leads to apoptosis. Pro-survival proteins belonging to the BCL-2 family (BCL-X, MCL-1, BCL-2) rescue cells from such events and are a major factor in both normal and malignant B cells’ physiology. Detailed analysis of the mechanisms of action of such antiapoptotic proteins is beyond the scope of this review and will therefore not be discussed further. Adapted from “Electron Transport Chain”, by BioRender.com (2020). Retrieved from https://app.biorender.com/biorender-templates (accessed on 6 July 2021).