Area of research
Molecular Biology · Physiology
Research interest
Research interests include Mitochondrial Function and Pathology, Metabolism and Genetic Disorders, Adipose Tissue and Metabolism, and ATP Synthase and ATPases Research.
Rescuing Ischemic Brain Injury by Rewiring Mitochondrial Electron Flow
HIF1α stabilization in hypoxia is not oxidant-initiated
Mitochondrial Dysfunction and Permeability Transition in Neonatal Brain and Lung Injuries
Mildronate protects heart mtDNA from oxidative stress toxicity induced by exhaustive physical exercise.
Crosstalk between the mTOR and Nrf2/ARE signaling pathways as a target in the improvement of long-term potentiation
p62-Nrf2-p62 Mitophagy Regulatory Loop as a Target for Preventive Therapy of Neurodegenerative Diseases
INTEGRAL ANALYSIS OF GENOMIC AND TRANSCRIPTOMIC CHANGES IN CLEAR CELL RENAL CELL CARCINOMA IN THE RUSSIAN POPULATION
Autophagy Induction by Bexarotene Promotes Mitophagy in Presenilin 1 Familial Alzheimer’s Disease iPSC-Derived Neural Stem Cells
Redox-Dependent Loss of Flavin by Mitochondrial Complex I in Brain Ischemia/Reperfusion Injury
Autophagy Induction by Bexarotene Promotes Mitophagy in Presenilin 1 Familial Alzheimer's Disease iPSC-Derived Neural Stem Cells.
Redox-Dependent Loss of Flavin by Mitochondrial Complex I in Brain Ischemia/Reperfusion Injury.
Methylene blue does not bypass Complex III antimycin block in mouse brain mitochondria.
Unique features of flight muscles mitochondria of honey bees (Apis mellifera L.).
Benfotiamine treatment activates the Nrf2/ARE pathway and is neuroprotective in a transgenic mouse model of tauopathy
Distinct Nrf2 Signaling Mechanisms of Fumaric Acid Esters and Their Role in Neuroprotection against 1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine-Induced Experimental Parkinson's-Like Disease
Discovery of LRE1 as a specific and allosteric inhibitor of soluble adenylyl cyclase
Mitochondrial ROS metabolism: 10 Years later
Methylene blue upregulates Nrf2/ARE genes and prevents tau-related neurotoxicity
Scavenging of H2O2 by mouse brain mitochondria
The Oxygen Free Radicals Originating from Mitochondrial Complex I Contribute to Oxidative Brain Injury Following Hypoxia–Ischemia in Neonatal Mice
Hypoxic-Ischemic Injury in the Developing Brain: The Role of Reactive Oxygen Species Originating in Mitochondria