Reversal of mitochondrial dysfunction

Mitochondria are the powerhouses of the cell. The functioning of all cells of the body is associated with their effective work. They are especially important for the most energy-consuming organs, including brain, retina, kidneys, skeletal muscles and myocardium. Increasing levels of mitochondrial ROS in dysfunctional mitochondria inactivates the enzyme glyceraldehyde-3 phosphate dehydrogenase (GAPDH), that is necessary for the utilization of glucose in the energy metabolism of a cell. This leads to the accumulation of products the metabolism of which is harmful to a cell as glyoxal and methyl glyoxal. The cell then releases advanced glycation end products (AGEs). Receptor of advanced glycation end products (AGE receptor, RAGE) is present on macrophages, endothelial cells, and vascular smooth muscle cells. Its activation can cause chronic vascular inflammation such as atherosclerosis – which is a common condition for older people. RAGE inhibitor significantly suppressed AGES-RAGE-induced atherogenic activity of macrophages, their invasion into the vessel and absorption of oxidized low-density lipoprotein. It also induced AGE activation of NF-κB and increased expression of inflammatory genes, which leads to atherosclerotic foamy cells.
We aim to search for target genes, causing mitochondrial dysfunction and work on preventing it.

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