My research interests are focused on clinically relevant basic redox mechanisms of brain injury. In particular, my laboratory attempts to decipher novel pathogenic mechanisms through which oxidative and nitrosative stress participate in the evolution of secondary damage after acute brain injury. Presently, we are studying mitochondrial lipid signaling pathways involved in neuronal death. Our conceptual platform is based on the fact that mitochondria, while indispensable for aerobic life in eukaryotic cells, when dysregulated generate reactive oxygen species and subsequently generate oxidatively modified biomolecules that act as signals, mediators capable of killing neurons. Among the specific achievements, we have identified cardiolipin as the major regulator of mitochondrial biology via changes in its asymmetry and externalization as an “eat-me” signal for the elimination of damaged mitochondria in neurons. By applying lipidomics and oxidative lipidomics analysis, we discovered the non-random mechanisms and pathways of lipid peroxidation caused by traumatic and ischemic brain injury. We found that selective oxidative metabolism of polyunsaturated cardiolipins leading to accumulation of >150 new oxygenated molecular species of cardiolipin — rather than non-specific oxidation of more abundant phospholipids — was involved in pathogenic pathways of injury. Elimination of cardiolipin oxidation by newly designed classes of mitochondria-targeted regulators showed great effectiveness in preventing neurological damage. Deciphering the meaning of these oxygenated cardiolipin-derived signals represents one of the current research areas.