Abstract
Mitochondria are organelles with highly dynamic ultrastructure maintained by flexible fusion and fission rates governed by Guanosine Triphosphatases (GTPases) dependent proteins. Balanced control of mitochondrial quality control is crucial for maintaining cellular energy and metabolic homeostasis; however, dysfunction of the dynamics of fusion and fission causes loss of integrity and functions with the accumulation of damaged mitochondria and mitochondrial deoxyribose nucleic acid (mtDNA) that can halt energy production and induce oxidative stress. Mitochondrial derived reactive oxygen species (ROS) can mediate redox signaling or, in excess, causing activation of inflammatory proteins and further exacerbate mitochondrial deterioration and oxidative stress. ROS have a deleterious effect on many cellular components, including lipids, proteins, both nuclear and mtDNA and cell membrane lipids producing the net result of the accumulation of damage associated molecular pattern (DAMPs) capable of activating pathogen recognition receptors (PRRs) on the surface and in the cytoplasm of immune cells. Chronic inflammation due to oxidative damage is thought to trigger numerous chronic diseases including cardiac, liver and kidney disorders, neurodegenerative diseases (Parkinson's disease and Alzheimer's disease), cardiovascular diseases/atherosclerosis, obesity, insulin resistance, and type 2 diabetes mellitus.