Alexander Galkin, Ph.D.

Energy generation and conversion in our body are mainly driven by mitochondria. Most of the oxygen from the air we breathe is consumed by mitochondria in the process of energy production called cellular respiration.  A timely and sufficient energy supply is critical for the development and maintenance of highly metabolizing tissues, such as the brain and heart. Energy production in mitochondria would not be possible without oxygen, so lack of oxygen, or hypoxia, can damage cells and tissues. Hypoxia can be caused by many factors including disease, pathology, or trauma, and can occur during surgery or organ transplantation. Usually, hypoxia is followed by restoration of oxygen supply (reoxygenation), which makes the damage greater and in some cases irreversible. Mitochondria are not the only sites of injury during this process, however, they are also mainly responsible for that damage as they form toxic agents known as Reactive Oxygen Species (ROS). 

We combine our unique expertise in mitochondrial physiology and metabolism, enzymology, molecular biology, and medicine to gain a better knowledge of pathological conditions during ischemia/reperfusion when mitochondria are affected. Together with our collaborators and BMRI and WCM, we use our knowledge of the structure and function of mitochondrial enzymes to analyze the effect of various pathological conditions on energy metabolism.

The main goal of our laboratory is to find new bioenergetic mechanisms behind the changes that occur during human pathologies and to apply this knowledge to the design of novel therapeutic approaches in clinical practice.


Recent publications:

Active Funding: 

“Metаbоlic оrigin of оxidаtive stress injury in brаin ischemiа/reperfusiоn”  R21
“The rоle of FMN lоss by mitochondriаl Complex I in neоnаtal hypоxic-ischemic brаin injury”, R01

Weill Cornell Medicine Mitochondria and Neurodegeneration Lab 407 East 61st Street, 5th Floor New York, NY 10065 Phone: (646) 962-8271