Asst. Prof. Dr. Şükrü Anıl Doğan

Mitochondria use oxygen to convert energy from nutrients into the cell’s major energy currency, ATP, through oxidative phosphorylation (OXPHOS). Because of their essential role in bioenergetics, impairment of mitochondria can lead to severe, often tissue-specific, disorders. Cells have developed various kinds of compensatory mechanisms, i.e. mitochondrial biogenesis, to counteract mitochondrial dysfunction, which play a central role in determining the extent of tissue-specific defects of disease phenotypes. In spite of recent progress, no specific therapy is currently available for OXPHOS disorders.

As the chief consumers of intracellular oxygen, mitochondria are the main source of reactive oxygen species (ROS), which are now being appreciated to have useful and beneficial effects such as signaling. ROS signaling controls a large number of transcriptional pathways; however, its importance in vivo has not been adequately investigated. When the redox equilibrium is disturbed due to the excessive accumulation or depletion of ROS, many cellular signaling pathways are influenced which confers to the cellular dysfunction and subsequently the development of various pathologies.

Currently, ROS-lowering interventions (such as antioxidants) are widely proposed as an anti-aging strategy in humans and used widely as therapy in some diseases. However, reducing the signaling ROS might be detrimental in some cases. We need to understand the under-studied physiological roles of ROS signaling to design better therapies for diseases and underline the potential hazards of unnecessary antioxidant use/treatment.