SECONDARY MITOCHONDRIAL DYSFUNCTION

Mitochondria are the most vital organelle in the cell because of its multitask properties. They are well known for the production of energy in the form of adenosine triphosphate (ATP) through oxidative phosphorylation (OXPHOS), which involves multiple complexes and cofactors. Mitochondria in addition to ATP production, also perform other vital functions like generation of reactive oxygen species (ROS), antioxidants, apoptosis, signaling and hormone actions. Because of their multiple actions, it is quite expected that their dysfunction will result in the number of effects. Since most vital organs exclusively depend on ATP to perform their functions, therefore impediment in its supply resulting from mitochondrial dysfunction will be detrimental and have a widespread spectrum. Neurodegenerative disorders, Huntington’s disease, cardiovascular disease (CVD), epilepsy, aging, metabolic syndrome, diabetes, autism, muscular atrophy, lou gehrig’s disease, neoplasia, down syndrome are few instances where mitochondrial dysfunction is the basic cause in pathogenesis. Mitochondrial disorders are either Primary or secondary disorders. Primary mitochondrial disease or disorder (PMD) has mitochondrial or nuclear deoxyribonucleic acid (mt DNA or nDNA) mutation affecting oxidative phosphorylation (OXPHOS). While Secondary mitochondrial dysfunction (SMD) does not involve OXPHOS but is the result of mutations in non OXPHOS genes. Secondary mitochondrial dysfunction (SMD) can also be acquired secondary to adverse factors those cause oxidative stress. All this highlights the role of mitochondria and makes it a new therapeutic target in managing these disorders. The present review has briefly discussed the secondary mitochondrial dysfunctional disorders and the approach to tackle it