Mitochondrial Dysfunction Contributes to Hypertensive Target Organ Damage: Lessons from an Animal Model of Human Disease

Figure 1

Schematic representation of the electron transport chain OXPHOS within the inner mitochondrial membrane. Complex I is highlighted to underscore its major relevance as a determinant of excessive mitochondrial ROS production when it becomes dysfunctional. In particular, lack of Ndufc2 subunit of complex I is highlighted to indicate that it leads to disassembly and dysfunction of the complex. As a result, NADH cannot be converted to NAD⁺, with consequent reduction of the flux of protons into the matrix, significant decrease of mitochondrial membrane potential, increase of anion superoxide, and reduction of ATP synthesis. The resulting cellular and tissue damage can contribute to target organ damage development in hypertension.