Mitochondrial Dysfunction as a Therapeutic Target in COPD

Mitochondria are key regulators of metabolism, redox homeostasis, and cell survival and proliferation. They are the most important source of intracellular reactive oxygen species generated during the synthesis of ATP through oxidative phosphorylation, and mitochondrial reactive oxygen species (mtROS) are key regulators of mitochondrial function. Failure to scavenge mtROS leads to mitochondrial dysfunction as shown in airway epithelial cells exposed to CSE leading to decreased ATP levels and mitochondrial membrane potential and impaired mitophagy. In addition, mitochondrial fragmentation, branching and reduced cristae are linked to increased levels of IL-6, CXCL8 and IL-1β and to senescence features